STUDY - Technical - New Dacian's Medicine
Diarrhea
(2)
Translation Draft
So, let me present some elements about differential diagnosis! Potentially, any medication can cause diarrhea and a careful drug history should be obtained from any patient with acute diarrhea. Other ingested toxins should also be considered, including organophosphoric insecticides, fungi, arsenic and even caffeine. Acute diverticulitis can sometimes present with diarrhea accompanied by fever and abdominal pain.
In patients with acute bloody diarrhoea, diagnostic reasoning may include thrombosis of the upper mesenteric artery or vein, drug-induced or ischemic colitis or idiopathic inflammatory bowel disease (ulcerative colitis or Crohn's disease). In the elderly patient with acute colitis, differentiating an ischemic cause of enterohemorrhagic E. coli may be difficult, as both diseases may be associated with submucous haemorrhage posing as a "finger fingerprint" on a simple abdominal X-ray.
While colonoscopic and radiographic signals may be apparent in infectious colitis and inflammatory bowel disease, histological results may be useful in suggesting one diagnosis or another, since inflammatory infiltration into acute infectious diarrhea consists mainly of polymorphonuclear leukocytes, rather than chronic inflammatory infiltration with distortions of crypts, typical for inflammatory bowel disease. The presence of pseudomembranes at colonoscopy indicates C. difficile as the cause.
It's the "turn" of the lab diagnosis... Acute infectious diarrhea is usually self-limiting, often healing until the patient requests medical attention. Due to the cost of coprocultures and other diagnostic tests, thorough judgment is required to decide which patients with acute diarrhoea should be evaluated and treated with antibiotics. For patients who present without high fever, bloody diarrhoea or dehydration, symptomatic therapy with fluids per bone in the absence of specific diagnostic investigations may be sufficient.
On the other hand, high fever, systemic toxicity, bloody diarrhea and dehydration tend towards diagnostic investigation, as happens in a known epidemic of food poisoning, recent distant travel, immunodeficiencies, male homosexuality or recent use of antibiotics. In these situations, the freshly harvested stool should be examined for occult haemorrhages and leukocytes.
The mainly detecting of polymorphonuclear leukocytes at a Wright or methylene blue coloration suggests Salmonella, Shigella, Invasive E. coli, Yersinia or Entamoeba histolytica. Although it is common practice to obtain a quantitative determination of faecal fats in patients with acute diarrhoea, the presence of small amounts of lipids in the stool is not unusual in patients with acute diarrhoea of any cause and does not provide particular diagnostic information. The key to diagnosis in patients with severe diarrhoea, especially bloody or suggestive epidemiological history, is bacterial culture and microscopic examination of egg and parasite stools.
Most laboratories routinely examine fecal samples sent for cultivation for Salmonella, Shigella, Yersinia and Campylobacter, but express request should be made to identify other microorganisms, including C. difficile (culture and toxin) and enterohemorrhagic E. coli. Special cultivation or special colouring techniques are also necessary for the identification of microorganisms causing watery diarrhea, including Aeromonas, Cryptosporidium and Vibrio species.
Certain microorganisms, such as Giardia Lamblia and Strongyloides, such as Cryptosporidium and Isospora belli can be difficult to detect in the stool and are better diagnosed by duodenal suction or intestinal biopsy. Alternatively, a sensitive and specific analysis, by binding enzyme immunoabsorption (linked) for the Antigen Giardia in faeces, can be used to confirm giardiosis. In AIDS patients, the electron microscopy examination of small intestine biopsies may facilitate the detection of Microsporidia.
Sigmoidoscopy and sometimes colonoscopy are generally reserved for patients with bloody diarrhoea, which does not improve within 10 days. As discussed above, mucosal changes may be nonspecific, although in some cases characteristic features may be observed, such as pseudomembranes in C. difficile - induced colitis. Barium X-rays are also preferably postponed until the initial course of the disease has been observed and stool samples have been obtained. Even after the application of all available laboratory investigations, between 20 and 40% of all forms of acute infectious diarrhoea remain undiagnosed.
General and non-specific treatment of acute infectious diarrhea includes rest and fluid replacement. Since death in most cases of acute diarrhoea occurs through dehydration, special attention should be paid to the correction of electrolyte deficits. Intravenous fluid therapy may be necessary in severely dehydrated individuals, especially children and the elderly. Electrolyte solutions administered per bone, used in the treatment of patients with cholera, may also be considered in patients with acute diarrhoea due to other enterotoxin-producing bacteria.
Antibiotic therapy in bacterial diarrhea is controversial and is generally not necessary in patients with mild or healing disease, but should be considered in patients with shigelosis, traveler's diarrhea, pseudomembranous enterocolitis, cholera and parasitic diseases. Regardless of the cause of infectious diarrhoea, patients should be treated if they are immunocompromised, have a malignant disease, have an abnormal heart valve or vascular or orthopedic prostheses, have hemolytic anaemia, are very young or very old.
Anticholinergic drugs and opiates should generally be avoided in the treatment of diarrhoea when an enteroinvasive microorganism is suspected, due to the risk of prolonging colonisation or producing an ileeus. However, loperamide and bismuth subsalicylate have proven effective for patients with traveller's diarrhoea, who have neither high fever nor blood or pus in the stool.
We can now move on to presentations on chronic diarrhea. Diarrhea that persists for weeks or months, either constant or intermittent, requires investigation. Although in most cases the cause will prove to be irritable bowel syndrome, diarrhea is a manifestation of a serious underlying disease and a careful search for an organic disease should be undertaken. Chronic diarrhea can be classified physiopathologically in osmotic diarrhea (malabsorption), secretory diarrhea, diarrhea due to disorders of intestinal motility and artificial diarrhea.
Inflammatory diares are generally characterized by the presence of fever, abdominal sensitivity and blood or leukocytes in the stool, with inflammatory lesions on the biopsy of the intestinal mucosa. In some lesions, hypoalbuminemia, hypoglobulinemia and enteropathy with loss of protein may be present. In addition to inflammation, the mechanism of diarrhea may include malabsorption or increased intestinal secretion.
In a patient who does not have a systemic disease, a liquid stool with occult or obvious bleeding raises the possibility of colon cancer. Patients with ulcerative proctitis may also present with such stools. In a patient with systemic disease and chronic bloody diarrhea, the diagnosis of inflammatory bowel disease (either ulcerative colitis or Crohn's disease) is suggested. These conditions should also be suspected when chronic diarrhoea is associated with important extraintestinal manifestations, including arthritis, skin lesions (such as erythema nodos or gangrenous pyoderma), uveitis or vasculitis.
Diarrhea in inflammatory bowel disease can result from lesions of the absorbative surface epithelium, as well as from the release into circulation of secretagogs like leukotrienes, prostaglandins, histamine and other cytokines that stimulate intestinal secretion or enteric nervous system. Inflammatory diarrhea is found in patients with chronic irradiation enterocolitis as a result of pelvic irradiation for malignant diseases of the female or male urogenital tract (prostate). The affected segments are usually the terminal ileum, the check and the rectosigmoid, because they are fixed in the pelvis.
The risk of irradiation enterocolitis correlates with the radiation dose. Chronic irradiation lesion is characterized by progressive swelling of endothelial cells in the small arterioles of the submucosa, leading to obliterating endarteritis and vascular thrombosis and causing ischemia with fibrosis, thickening of the intestinal wall, ulceration and cracking of the mucosa. Colonoscopy may show light narrowing, ulceration, diffuse inflammatory changes and characteristic mucous telangiectasis that may bleed severely. Diarrhea can also result from malabsorption of bile acids due to ileal inflammation or bacterial proliferation under conditions of strictures or intestinal stasis.
Eosinophilic gastroenteritis is characterized by infiltration of any portion of the gastrointestinal tract with eosinophils. In addition to diarrhoea, patients experience abdominal pain, nausea, vomiting, weight loss and in 75% of cases, peripheral eosinophilia (some patients may experience steatorea and enteropathy with loss of protein). Severe enteropathy with protein loss is manifested by peripheral edema, ascites and sometimes anasarca.
It can occur in various pathological conditions, including infections (viral gastroenteritis, bacterial proliferation, parasitic infestation, enterocolitis with C. difficile or Whipple's disease), inflammatory bowel disease, splanchinic congestion due to heart failure, lymphomas or other diseases associated with lymphatic obstruction, such as congenital intestinal lymphangiectasis, Menetrier's disease, systemic lupus erythematosus or milk allergy.
Recently, an increasing number of infectious causes of chronic diarrhea have been associated with infections caused by human immunodeficiency virus (HIV) or AIDS. In many patients with AIDS and diarrhoea, multiple pathogens may be present in stools, although the precise cause of diarrhea may be uncertain because such pathogens can also be found in the stool of HIV patients without diarrhea. It is assumed that the HIV virus itself causes diarrhea in certain cases (AIDS enteropathy), but the mechanism is not yet understood.
Other various diseases associated with inflammatory diarrhea include Behcet syndrome and graft-versus-host syndrome after allogeneic bone marrow transplantation.
I will complete this post with presentations on osmotic diarrhea. This occurs when a dissolved substance ingested orally is not fully absorbed into the small intestine and therefore exerts an osmotic force that causes the fluid into the intestinal lumen. The increased volume of the luminal fluid exceeds the reabsorption capacity of the colon. Unabsorbed solvent may be a nutrient or a maldigested or malabsorbed medicine.
Clinical symptoms are usually recognized due to malabsorption of lipids (steatorea) or carbohydrates. Malabsorption of proteins or amino acids (azotorea) is generally not clinically recognized unless it is severe enough to cause malnutrition or the consequences of a specific deficiency of an amino acid.
Intraluminal maldigestion can result from exocrine pancreatic insufficiency, which occurs when at least 90% of the secretory capacity of the pancreas is lost, in patients with chronic pancreatitis or sometimes with pancreatic ductal obstruction. Maldigestion and weight loss occur despite the retained appetite. In children, cystic fibrosis or Schwachman syndrome can cause chronic pancreatic insufficiency.
Somatostatinoma is a rare tumor of the pancreatic islands that leads to biliary lithiasis, diabetes and steatorea, which is believed to be caused by inhibition of pancreatic secretion. Intraluminal maldigestion can also result from obstruction of the bile ducts as a result of pancreatic head cancer or from serious liver disease with cholestasis. Deficiency of intraluminal bile salts usually causes only a mild malabsorption of fats.
Bacterial hyperproliferation in a blind bowel or stasis segment (e.g. due to an enterocolic tissue, jejunal diverticulosis, intestinal dysmotility due to scleroderma, diabetes or chronic intestinal pseudoobstruction) can cause steatorea due to deconjugation of bile salts and damage to the formation of myceliums (additional factors leading to diarrhea are the destruction of edge enzymes in the brush, inflammation of the mucosa, hydroxylation of lipids causing di fatty acids).
Osmotic diarrhea can result from chronic ingestion of certain fruits or candy, gum, dietary foods and medicines sweetened with unabsorbed carbohydrates like sorbitol or fructose. The congenital absence of hydrolases for carbohydrates and transport proteins from the edge to the brush can also lead to chronic diarrhea (the most common of these is lactase deficiency causing lactose intolerance).
The classic example of mucous malabsorption is celiac sprue or gluten-sensitive enteropathy. In addition to typical symptoms and signs of malabsorption, the patient with celiac sprue may show atypical signs, including developmental incapacity, muscle "melting", abdominal distension and irritability in young children and ferriprivate anaemia, increasing retardation and anorexia in adolescents or young adults. Later in life, patients may present with nutritionally csidious deficits, sterility and neuromuscular diseases.
Like celiac sprue, tropical sprue is characterized by malabsorption and histological changes in the small intestine; villi atrophy, hyperplasia of the crypts, damaged surface epithelium and a mononuclear infiltration into the lamina itself. A disease affecting the inhabitants of certain tropical regions of the world, tropical sprue can occur even in visitors who have spent only 1-3 months in an endemic area. The onset may be acute, suggesting an infectious etiology.
Intestinal malabsorption is typical of Whipple's disease due to Tropheryma whipping, which usually affects middle-aged men, but can be found at any age and in patients of both sexes. Additional manifestations include arthralgia, fever and chills, hypotension, adenopathy and damage to the central nervous system. Abetalipoproteinemia is caused by the absence of Apo B leading to defective formation of chilomicrons.
Children with this disorder have steatorea, acantocytic erythrocytes, ataxia and retinitis pigmentosa. Steatorea may also be the result of infection with Giardia Lamblia, Isospora, Strongyloides and complex Mycobacterium avium. Ingestion of certain medicines can cause steatorea due to damage to erythrocytes (e.g. colchicine, neomycin and paraaminosalicylic acid).
Intestinal lymphangiectasis causes enteropathy with protein loss and steatorea, but with retained carbohydrate absorption and is thus an example of post-mucous obstruction of the lymphatic canals. The disease can be congenital or acquired as a result of trauma, carcinomas or Whipple's disease.
Finally, extensive intestinal resection can cause short bowel syndrome, in which steatorea results from an inadequate absorption surface, low transit time and low amount of bile salts. Other factors that may contribute to diarrhea in short bowel syndrome include the osmotic effect of unabsorbed dissolved substances, gastric hypersecretion and, in some cases, bacterial proliferation.
Ready for today! On Sunday 22 June I will complete the posts about diarrhea and I will be able to cool to constipation.
So, let me present some elements about differential diagnosis! Potentially, any medication can cause diarrhea and a careful drug history should be obtained from any patient with acute diarrhea. Other ingested toxins should also be considered, including organophosphoric insecticides, fungi, arsenic and even caffeine. Acute diverticulitis can sometimes present with diarrhea accompanied by fever and abdominal pain.
In patients with acute bloody diarrhoea, diagnostic reasoning may include thrombosis of the upper mesenteric artery or vein, drug-induced or ischemic colitis or idiopathic inflammatory bowel disease (ulcerative colitis or Crohn's disease). In the elderly patient with acute colitis, differentiating an ischemic cause of enterohemorrhagic E. coli may be difficult, as both diseases may be associated with submucous haemorrhage posing as a "finger fingerprint" on a simple abdominal X-ray.
While colonoscopic and radiographic signals may be apparent in infectious colitis and inflammatory bowel disease, histological results may be useful in suggesting one diagnosis or another, since inflammatory infiltration into acute infectious diarrhea consists mainly of polymorphonuclear leukocytes, rather than chronic inflammatory infiltration with distortions of crypts, typical for inflammatory bowel disease. The presence of pseudomembranes at colonoscopy indicates C. difficile as the cause.
It's the "turn" of the lab diagnosis... Acute infectious diarrhea is usually self-limiting, often healing until the patient requests medical attention. Due to the cost of coprocultures and other diagnostic tests, thorough judgment is required to decide which patients with acute diarrhoea should be evaluated and treated with antibiotics. For patients who present without high fever, bloody diarrhoea or dehydration, symptomatic therapy with fluids per bone in the absence of specific diagnostic investigations may be sufficient.
On the other hand, high fever, systemic toxicity, bloody diarrhea and dehydration tend towards diagnostic investigation, as happens in a known epidemic of food poisoning, recent distant travel, immunodeficiencies, male homosexuality or recent use of antibiotics. In these situations, the freshly harvested stool should be examined for occult haemorrhages and leukocytes.
The mainly detecting of polymorphonuclear leukocytes at a Wright or methylene blue coloration suggests Salmonella, Shigella, Invasive E. coli, Yersinia or Entamoeba histolytica. Although it is common practice to obtain a quantitative determination of faecal fats in patients with acute diarrhoea, the presence of small amounts of lipids in the stool is not unusual in patients with acute diarrhoea of any cause and does not provide particular diagnostic information. The key to diagnosis in patients with severe diarrhoea, especially bloody or suggestive epidemiological history, is bacterial culture and microscopic examination of egg and parasite stools.
Most laboratories routinely examine fecal samples sent for cultivation for Salmonella, Shigella, Yersinia and Campylobacter, but express request should be made to identify other microorganisms, including C. difficile (culture and toxin) and enterohemorrhagic E. coli. Special cultivation or special colouring techniques are also necessary for the identification of microorganisms causing watery diarrhea, including Aeromonas, Cryptosporidium and Vibrio species.
Certain microorganisms, such as Giardia Lamblia and Strongyloides, such as Cryptosporidium and Isospora belli can be difficult to detect in the stool and are better diagnosed by duodenal suction or intestinal biopsy. Alternatively, a sensitive and specific analysis, by binding enzyme immunoabsorption (linked) for the Antigen Giardia in faeces, can be used to confirm giardiosis. In AIDS patients, the electron microscopy examination of small intestine biopsies may facilitate the detection of Microsporidia.
Sigmoidoscopy and sometimes colonoscopy are generally reserved for patients with bloody diarrhoea, which does not improve within 10 days. As discussed above, mucosal changes may be nonspecific, although in some cases characteristic features may be observed, such as pseudomembranes in C. difficile - induced colitis. Barium X-rays are also preferably postponed until the initial course of the disease has been observed and stool samples have been obtained. Even after the application of all available laboratory investigations, between 20 and 40% of all forms of acute infectious diarrhoea remain undiagnosed.
General and non-specific treatment of acute infectious diarrhea includes rest and fluid replacement. Since death in most cases of acute diarrhoea occurs through dehydration, special attention should be paid to the correction of electrolyte deficits. Intravenous fluid therapy may be necessary in severely dehydrated individuals, especially children and the elderly. Electrolyte solutions administered per bone, used in the treatment of patients with cholera, may also be considered in patients with acute diarrhoea due to other enterotoxin-producing bacteria.
Antibiotic therapy in bacterial diarrhea is controversial and is generally not necessary in patients with mild or healing disease, but should be considered in patients with shigelosis, traveler's diarrhea, pseudomembranous enterocolitis, cholera and parasitic diseases. Regardless of the cause of infectious diarrhoea, patients should be treated if they are immunocompromised, have a malignant disease, have an abnormal heart valve or vascular or orthopedic prostheses, have hemolytic anaemia, are very young or very old.
Anticholinergic drugs and opiates should generally be avoided in the treatment of diarrhoea when an enteroinvasive microorganism is suspected, due to the risk of prolonging colonisation or producing an ileeus. However, loperamide and bismuth subsalicylate have proven effective for patients with traveller's diarrhoea, who have neither high fever nor blood or pus in the stool.
We can now move on to presentations on chronic diarrhea. Diarrhea that persists for weeks or months, either constant or intermittent, requires investigation. Although in most cases the cause will prove to be irritable bowel syndrome, diarrhea is a manifestation of a serious underlying disease and a careful search for an organic disease should be undertaken. Chronic diarrhea can be classified physiopathologically in osmotic diarrhea (malabsorption), secretory diarrhea, diarrhea due to disorders of intestinal motility and artificial diarrhea.
Inflammatory diares are generally characterized by the presence of fever, abdominal sensitivity and blood or leukocytes in the stool, with inflammatory lesions on the biopsy of the intestinal mucosa. In some lesions, hypoalbuminemia, hypoglobulinemia and enteropathy with loss of protein may be present. In addition to inflammation, the mechanism of diarrhea may include malabsorption or increased intestinal secretion.
In a patient who does not have a systemic disease, a liquid stool with occult or obvious bleeding raises the possibility of colon cancer. Patients with ulcerative proctitis may also present with such stools. In a patient with systemic disease and chronic bloody diarrhea, the diagnosis of inflammatory bowel disease (either ulcerative colitis or Crohn's disease) is suggested. These conditions should also be suspected when chronic diarrhoea is associated with important extraintestinal manifestations, including arthritis, skin lesions (such as erythema nodos or gangrenous pyoderma), uveitis or vasculitis.
Diarrhea in inflammatory bowel disease can result from lesions of the absorbative surface epithelium, as well as from the release into circulation of secretagogs like leukotrienes, prostaglandins, histamine and other cytokines that stimulate intestinal secretion or enteric nervous system. Inflammatory diarrhea is found in patients with chronic irradiation enterocolitis as a result of pelvic irradiation for malignant diseases of the female or male urogenital tract (prostate). The affected segments are usually the terminal ileum, the check and the rectosigmoid, because they are fixed in the pelvis.
The risk of irradiation enterocolitis correlates with the radiation dose. Chronic irradiation lesion is characterized by progressive swelling of endothelial cells in the small arterioles of the submucosa, leading to obliterating endarteritis and vascular thrombosis and causing ischemia with fibrosis, thickening of the intestinal wall, ulceration and cracking of the mucosa. Colonoscopy may show light narrowing, ulceration, diffuse inflammatory changes and characteristic mucous telangiectasis that may bleed severely. Diarrhea can also result from malabsorption of bile acids due to ileal inflammation or bacterial proliferation under conditions of strictures or intestinal stasis.
Eosinophilic gastroenteritis is characterized by infiltration of any portion of the gastrointestinal tract with eosinophils. In addition to diarrhoea, patients experience abdominal pain, nausea, vomiting, weight loss and in 75% of cases, peripheral eosinophilia (some patients may experience steatorea and enteropathy with loss of protein). Severe enteropathy with protein loss is manifested by peripheral edema, ascites and sometimes anasarca.
It can occur in various pathological conditions, including infections (viral gastroenteritis, bacterial proliferation, parasitic infestation, enterocolitis with C. difficile or Whipple's disease), inflammatory bowel disease, splanchinic congestion due to heart failure, lymphomas or other diseases associated with lymphatic obstruction, such as congenital intestinal lymphangiectasis, Menetrier's disease, systemic lupus erythematosus or milk allergy.
Recently, an increasing number of infectious causes of chronic diarrhea have been associated with infections caused by human immunodeficiency virus (HIV) or AIDS. In many patients with AIDS and diarrhoea, multiple pathogens may be present in stools, although the precise cause of diarrhea may be uncertain because such pathogens can also be found in the stool of HIV patients without diarrhea. It is assumed that the HIV virus itself causes diarrhea in certain cases (AIDS enteropathy), but the mechanism is not yet understood.
Other various diseases associated with inflammatory diarrhea include Behcet syndrome and graft-versus-host syndrome after allogeneic bone marrow transplantation.
I will complete this post with presentations on osmotic diarrhea. This occurs when a dissolved substance ingested orally is not fully absorbed into the small intestine and therefore exerts an osmotic force that causes the fluid into the intestinal lumen. The increased volume of the luminal fluid exceeds the reabsorption capacity of the colon. Unabsorbed solvent may be a nutrient or a maldigested or malabsorbed medicine.
Clinical symptoms are usually recognized due to malabsorption of lipids (steatorea) or carbohydrates. Malabsorption of proteins or amino acids (azotorea) is generally not clinically recognized unless it is severe enough to cause malnutrition or the consequences of a specific deficiency of an amino acid.
Intraluminal maldigestion can result from exocrine pancreatic insufficiency, which occurs when at least 90% of the secretory capacity of the pancreas is lost, in patients with chronic pancreatitis or sometimes with pancreatic ductal obstruction. Maldigestion and weight loss occur despite the retained appetite. In children, cystic fibrosis or Schwachman syndrome can cause chronic pancreatic insufficiency.
Somatostatinoma is a rare tumor of the pancreatic islands that leads to biliary lithiasis, diabetes and steatorea, which is believed to be caused by inhibition of pancreatic secretion. Intraluminal maldigestion can also result from obstruction of the bile ducts as a result of pancreatic head cancer or from serious liver disease with cholestasis. Deficiency of intraluminal bile salts usually causes only a mild malabsorption of fats.
Bacterial hyperproliferation in a blind bowel or stasis segment (e.g. due to an enterocolic tissue, jejunal diverticulosis, intestinal dysmotility due to scleroderma, diabetes or chronic intestinal pseudoobstruction) can cause steatorea due to deconjugation of bile salts and damage to the formation of myceliums (additional factors leading to diarrhea are the destruction of edge enzymes in the brush, inflammation of the mucosa, hydroxylation of lipids causing di fatty acids).
Osmotic diarrhea can result from chronic ingestion of certain fruits or candy, gum, dietary foods and medicines sweetened with unabsorbed carbohydrates like sorbitol or fructose. The congenital absence of hydrolases for carbohydrates and transport proteins from the edge to the brush can also lead to chronic diarrhea (the most common of these is lactase deficiency causing lactose intolerance).
The classic example of mucous malabsorption is celiac sprue or gluten-sensitive enteropathy. In addition to typical symptoms and signs of malabsorption, the patient with celiac sprue may show atypical signs, including developmental incapacity, muscle "melting", abdominal distension and irritability in young children and ferriprivate anaemia, increasing retardation and anorexia in adolescents or young adults. Later in life, patients may present with nutritionally csidious deficits, sterility and neuromuscular diseases.
Like celiac sprue, tropical sprue is characterized by malabsorption and histological changes in the small intestine; villi atrophy, hyperplasia of the crypts, damaged surface epithelium and a mononuclear infiltration into the lamina itself. A disease affecting the inhabitants of certain tropical regions of the world, tropical sprue can occur even in visitors who have spent only 1-3 months in an endemic area. The onset may be acute, suggesting an infectious etiology.
Intestinal malabsorption is typical of Whipple's disease due to Tropheryma whipping, which usually affects middle-aged men, but can be found at any age and in patients of both sexes. Additional manifestations include arthralgia, fever and chills, hypotension, adenopathy and damage to the central nervous system. Abetalipoproteinemia is caused by the absence of Apo B leading to defective formation of chilomicrons.
Children with this disorder have steatorea, acantocytic erythrocytes, ataxia and retinitis pigmentosa. Steatorea may also be the result of infection with Giardia Lamblia, Isospora, Strongyloides and complex Mycobacterium avium. Ingestion of certain medicines can cause steatorea due to damage to erythrocytes (e.g. colchicine, neomycin and paraaminosalicylic acid).
Intestinal lymphangiectasis causes enteropathy with protein loss and steatorea, but with retained carbohydrate absorption and is thus an example of post-mucous obstruction of the lymphatic canals. The disease can be congenital or acquired as a result of trauma, carcinomas or Whipple's disease.
Finally, extensive intestinal resection can cause short bowel syndrome, in which steatorea results from an inadequate absorption surface, low transit time and low amount of bile salts. Other factors that may contribute to diarrhea in short bowel syndrome include the osmotic effect of unabsorbed dissolved substances, gastric hypersecretion and, in some cases, bacterial proliferation.
Ready for today! On Sunday 22 June I will complete the posts about diarrhea and I will be able to cool to constipation.
Good thoughts,
understanding, love and gratitude be with us!
Dorin, Merticaru