STUDY - Technical - New Dacian's Medicine
Diarrhea
(1)
Translation Draft
Before proceeding to the description of these signs of the disease it is good to "review" some things about normal intestinal function, starting with the absorption and secretion of the intestinal fluids.
On a typical day enters the gastrointestinal tract around about 9 (nine) liters of fluids: 2 l by direct ingestion, 1 l as saliva, 2 l of gastric juice and 4 l as bile, pancreatic and small intestine secretions. When passing through the small intestine, 4-5 l of liquid are reabsorbed into the jejun and 3-4 l into the ileum. Therefore, about 1 l of residual fluid enters the colon, where 800 ml of additional are reabsorbed before passing into the rectum and discharge. Overall, the usual amount of liquid secreted in faeces is about 200 ml/ day.
In the gut, water absorption tracks active and passive absorption of sodium (Na+) and nutrients. In the small intestine, Na+ is co-transported with chlorine (Cl-) and nutritional principles like glucose, in the terminal ileum Na+ being co-transported by bile salts, and in the colon Na+ is absorbed through the Na+ channels and through the NaCl electrical absorption mechanism used in the small intestine. The cotransport mechanism for Na+ absorption and food principles depends in part on Na+ gradients on either side of the apical membrane of the intestinal epithelial cells created by the Na+, K+ - ATP pump of the laterobasal membrane.
The most clinically important is a transporter of the Na+ cotransporter - glucose from the small intestine. The absorption of glucose through this mechanism leads to the accumulation of glucose in the epithelial cell, followed by its movement through the laterobasal membrane through a facilitated transport mechanism, while Na+ is actively pumped through the laterobasal membrane by ATP-ase Na+, K+. Na+ absorption also promotes the absorption of Cl- through a paracellular pathway. Water absorption is passive for maintaining isoosmolarity in the intercellular space.
Because the mechanism of cotransport Na+ - glucose remains unaffected by most diarrheal diseases, the administration of a glucosaline solution is clinically useful in the therapy of diarrhea and dehydration, regardless of the causes. There are other co-transport mechanisms. A Na+ - Cl- co-transport mechanism is currently considered to consist of a Na+-H+ exchange transporter and a Cl- - HCO3-exchange transporter. This mechanism allows both Na+ and Cl to enter the cell in exchange with H+ and HCO3-. Additional transport mechanisms have been identified for potassium (K+), which can be absorbed in exchange with H+ and calcium (Ca2+), whose absorption is regulated by vitamin D and 1,25-dihydroxyvitamin D3, the hormone parothyroid, calcitonin and a number of calcium-binding proteins.
In addition to the absorption function, the intestine also has a secretory function. Cl- can be secreted by intestinal crypt cells through an electrogenic mechanism, with Na+, K+ and water passively following through tight junctions. HCO3- is secreted in the duodenum, in other parts of the small intestine and in the bile and pancreatic ducts. Due to the large acidic load in the stomach, the secreted HCO3 is diluted and present in relatively low concentrations. However, in the distal intestine, HCO3- progressively becomes the predominant anion, allowing the preservation of Cl-, probably through a mechanism of exchange Cl---HCO3- to the apical membrane of epithelial cells. Intracellular cyclic nutrients and ionized calcium (Ca2+) initiate and regulate the active secretion of Cl-.
Let's move on to colonic function now... As in the small intestine, there is a mechanism in the colon to absorb Na+. Na+ absorption is predominantly electrogenic as the absorbed Na+ ion is not accompanied by cation exchange or anion co-transport. Na+ enters the colonic epithelial cells through channels in the apical membrane and is pumped out through the laterobasal membrane by ATP-aza Na+, K+. Various neuronal and nonneuronal mediators regulate the transport and colonic motility of ions, but the precise mechanisms are not fully elucidated.
The colon and rectum are innervated by nerve fibers that release norepinephrine, acetylcholine and other neurotransmitters. Parasympathetic nerves stimulate peristaltic contractions and electrolyte secretion, while adrenergic tone inhibits cholinergic stimulation and increases electrolyte absorption. Additional adjustment is provided by local reflex arcs inside the enteric autonomic nervous system and intrinsic contractile responses of the smooth colonic muscle.
The defecation reflex is initiated by acute distension of the rectum, which causes partial and transient relaxation of the internal anal sphincter through parasympathetic innervation. While sigmoid and rectal contractions increase the pressure in the rectum, the retrosigmoid angle achieved by the tonic contraction of the puborectal muscle, which forms a chain around the ano-rectal junction, is erased.
The contraction of the external anal sphincter, which consists of at least three striated muscle bundles surrounding the anal canal and inervated by the shameful nerve, can delay the defecation to a socially acceptable time. Concomitant relaxation of the internal and external anal sphincters then allows the evacuation of faeces which can be accelerated by an increase in intraabdominal pressure achieved by the Valsalva maneuver.
It is only now that I have actually reached diarrhea and I will begin with its definition. In developed countries, the normal weight of an adult's stool is less than 200 g/ day, with fecal water being 60-85% by weight. Normal stools frequency ranges from 3/ week to 3/ day. Factors influencing stool weight, consistency and frequency include: dietary fiber content, sex (average daily stool weight in women is lower than in men), ingested medications and possibly exercise and stress.
Diarrhea is formally defined as an increase in the daily weight of the stool above 200 g. Typically, the patient may also describe an abnormal increase in the fluidity and frequency of the stools. Diarrhea should be distinguished from pseudodiarrhea or hyperdefecation, which is an increase in the frequency of defecation without an increase in the weight of the stools above normal, as occurs in patients with irritable bowel syndrome, proctitis or hyperthyroidism.
Diarrhea should also be differentiated from fecal incontinence, which is the involuntary release of rectal contents. Incontinence is more common when the stool is liquid than when it is solid and reflects abnormal functioning of the anorectal or pelvic muscle. Diarrhea is considered acute when it lasts up to 7-14 days and chronic when it lasts over 2-3 weeks.
Let's move on to acute diarrhea! The most common causes of acute diarrhea are infectious agents. In this case, not to mention the infectious agents and their "way" of acting, they have physiopathological mechanisms represented by: 1. production of toxins (preformed toxin, endotoxin and cytotoxin), 2. enteroadherence, 3. invasion of the mucosa (which may be minimal, variable or severe) and 4. systemic infection.
Acute diarrhea can also be caused by ingested medicines or toxins, chemotherapy, resumption of enteral feeding after prolonged fasting, after blockage of feces (overflow diarrhea) or in particular situations, such as marathon race. In addition, acute diarrhea may represent the onset of chronic diarrheal disease.
Infectious diarrhea is responsible for more than 5-8 million deaths annually in children under 5 years of age, especially in developing countries where acute infectious diarrhea is a major cause of protein-calorie malnutrition and dehydration. favourable factors include poor water sanitation and supply, lack of refrigeration, overpopulation and lack of personal hygiene, poverty, lack of access to health services and lack of education.
Even in advanced countries such as the US, significant economic losses are "attracted" to acute infectious diarrhea that is responsible for 250,000 hospitalizations and nearly 8 million outpatient medical consultations annually. Most infectious diarrheals are acquired through fecal-oral transmission through water or food contaminated with human waste as a result of inadequate sewage systems or through feces of wild or domesticated animals in inadequately filtered water. Beef, pork or poultry can be a source of infection when prepared inappropriately.
The surfaces on which food is prepared may be contaminated by microorganisms that are transmitted to uncooked food. Person-to-person transmission can also occur through aerosolization (Norwalk agent, rotaviruses), contamination of hands (Clostridium difficile) or surfaces, or, including, through sexual activity. Particularly high risk groups for acute infectious diarrhoea also include tourists, people who ingest shellfish, gay men (homosexual bowel syndrome), prostitutes and intravenous drug users. People with AIDS in particular are at risk for a lot of serious enteric infections.
Among children who attend daycare centers, acute infectious diarrhea usually results from person-to-person transmission. The most common pathogens involved in diarrhoea epidemics in daytime care centres are Shigella, Giardia lamblia and Cryptosporidium. The secondary epidemic rate between 20-30% is an important source of infections for parents and siblings. Other institutions at high risk for the outbreak of acute infectious diarrhoea include institutes of care for the mentally and developmentally disabled, sanatoriums and hospitals.
I will complete this post with a few presentations about clinical features. Patients with acute infectious diarrhoea usually present with nausea, vomiting, abdominal pain, fever and diarrhoea, which may be watery, malabsorbent or bloody, depending on the specific pathogen. Patients who have ingested toxins or those with toxicogenic infection usually have nausea and vomiting as the main symptoms, but rarely high fever. Abdominal pain is mild, diffuse and colicative and comes from large volumes of secreted fluid that stimulates peristaltic and causes watery diarrhea.
Vomiting that begins a few hours after ingestion of a food suggests food poisoning due to a preformed toxin. Parasites that do not invade the intestinal mucosa, such as Giardia Lamblia and Cryptosporidium, usually cause only mild abdominal embarrassment. Giardia can also be associated with mild steatorea, meteorism and bloating. Invasive bacteria such as Campylobacter, Salmonella and Shigella, and cytotoxin agents such as Clostridium difficile and Escherichia Coli enterohemorrhagic, cause severe intestinal inflammation, abdominal pain and often high fever (sometimes peritoneal signs may suggest an acute abdomen).
Yersinia often infects the terminal ileum and the check and presents pain in the right iliac fossa and evocative sensitivity of acute appendicitis. Watery diarrhea is characteristic for microorganisms that invade the intestinal epithelium with minimal inflammation, such as enteric viruses, or microorganisms that adhere to but do not destroy the epithelium, such as enteropathogenic or enteroaderent E. coli, protozoa and helminths. Some microorganisms, such as Campylobacter, Aeromonas, Shigella and Vibrio, produce enterotoxins and invade the intestinal mucosa (patients therefore often present with watery diarrhea, followed within hours or days by bloody diarrhea).
The presence of systemic symptoms may provide additional clues to the underlying cause of diarrhea. Both shigelosis and enterohemorrhagic E. coli infection may be accompanied by hemolytic-uremic syndrome, especially in people who are very young or very elderly. Yersinia infection and occasionally other enteric bacterial infections may be accompanied by Reiter syndrome (arthritis, urethritis and conjunctivitis), thyroiditis, pericarditis or glomerulonephritis.
We continue the topic on June 20, addressing the differential diagnosis of acute diarrhea...
Before proceeding to the description of these signs of the disease it is good to "review" some things about normal intestinal function, starting with the absorption and secretion of the intestinal fluids.
On a typical day enters the gastrointestinal tract around about 9 (nine) liters of fluids: 2 l by direct ingestion, 1 l as saliva, 2 l of gastric juice and 4 l as bile, pancreatic and small intestine secretions. When passing through the small intestine, 4-5 l of liquid are reabsorbed into the jejun and 3-4 l into the ileum. Therefore, about 1 l of residual fluid enters the colon, where 800 ml of additional are reabsorbed before passing into the rectum and discharge. Overall, the usual amount of liquid secreted in faeces is about 200 ml/ day.
In the gut, water absorption tracks active and passive absorption of sodium (Na+) and nutrients. In the small intestine, Na+ is co-transported with chlorine (Cl-) and nutritional principles like glucose, in the terminal ileum Na+ being co-transported by bile salts, and in the colon Na+ is absorbed through the Na+ channels and through the NaCl electrical absorption mechanism used in the small intestine. The cotransport mechanism for Na+ absorption and food principles depends in part on Na+ gradients on either side of the apical membrane of the intestinal epithelial cells created by the Na+, K+ - ATP pump of the laterobasal membrane.
The most clinically important is a transporter of the Na+ cotransporter - glucose from the small intestine. The absorption of glucose through this mechanism leads to the accumulation of glucose in the epithelial cell, followed by its movement through the laterobasal membrane through a facilitated transport mechanism, while Na+ is actively pumped through the laterobasal membrane by ATP-ase Na+, K+. Na+ absorption also promotes the absorption of Cl- through a paracellular pathway. Water absorption is passive for maintaining isoosmolarity in the intercellular space.
Because the mechanism of cotransport Na+ - glucose remains unaffected by most diarrheal diseases, the administration of a glucosaline solution is clinically useful in the therapy of diarrhea and dehydration, regardless of the causes. There are other co-transport mechanisms. A Na+ - Cl- co-transport mechanism is currently considered to consist of a Na+-H+ exchange transporter and a Cl- - HCO3-exchange transporter. This mechanism allows both Na+ and Cl to enter the cell in exchange with H+ and HCO3-. Additional transport mechanisms have been identified for potassium (K+), which can be absorbed in exchange with H+ and calcium (Ca2+), whose absorption is regulated by vitamin D and 1,25-dihydroxyvitamin D3, the hormone parothyroid, calcitonin and a number of calcium-binding proteins.
In addition to the absorption function, the intestine also has a secretory function. Cl- can be secreted by intestinal crypt cells through an electrogenic mechanism, with Na+, K+ and water passively following through tight junctions. HCO3- is secreted in the duodenum, in other parts of the small intestine and in the bile and pancreatic ducts. Due to the large acidic load in the stomach, the secreted HCO3 is diluted and present in relatively low concentrations. However, in the distal intestine, HCO3- progressively becomes the predominant anion, allowing the preservation of Cl-, probably through a mechanism of exchange Cl---HCO3- to the apical membrane of epithelial cells. Intracellular cyclic nutrients and ionized calcium (Ca2+) initiate and regulate the active secretion of Cl-.
Let's move on to colonic function now... As in the small intestine, there is a mechanism in the colon to absorb Na+. Na+ absorption is predominantly electrogenic as the absorbed Na+ ion is not accompanied by cation exchange or anion co-transport. Na+ enters the colonic epithelial cells through channels in the apical membrane and is pumped out through the laterobasal membrane by ATP-aza Na+, K+. Various neuronal and nonneuronal mediators regulate the transport and colonic motility of ions, but the precise mechanisms are not fully elucidated.
The colon and rectum are innervated by nerve fibers that release norepinephrine, acetylcholine and other neurotransmitters. Parasympathetic nerves stimulate peristaltic contractions and electrolyte secretion, while adrenergic tone inhibits cholinergic stimulation and increases electrolyte absorption. Additional adjustment is provided by local reflex arcs inside the enteric autonomic nervous system and intrinsic contractile responses of the smooth colonic muscle.
The defecation reflex is initiated by acute distension of the rectum, which causes partial and transient relaxation of the internal anal sphincter through parasympathetic innervation. While sigmoid and rectal contractions increase the pressure in the rectum, the retrosigmoid angle achieved by the tonic contraction of the puborectal muscle, which forms a chain around the ano-rectal junction, is erased.
The contraction of the external anal sphincter, which consists of at least three striated muscle bundles surrounding the anal canal and inervated by the shameful nerve, can delay the defecation to a socially acceptable time. Concomitant relaxation of the internal and external anal sphincters then allows the evacuation of faeces which can be accelerated by an increase in intraabdominal pressure achieved by the Valsalva maneuver.
It is only now that I have actually reached diarrhea and I will begin with its definition. In developed countries, the normal weight of an adult's stool is less than 200 g/ day, with fecal water being 60-85% by weight. Normal stools frequency ranges from 3/ week to 3/ day. Factors influencing stool weight, consistency and frequency include: dietary fiber content, sex (average daily stool weight in women is lower than in men), ingested medications and possibly exercise and stress.
Diarrhea is formally defined as an increase in the daily weight of the stool above 200 g. Typically, the patient may also describe an abnormal increase in the fluidity and frequency of the stools. Diarrhea should be distinguished from pseudodiarrhea or hyperdefecation, which is an increase in the frequency of defecation without an increase in the weight of the stools above normal, as occurs in patients with irritable bowel syndrome, proctitis or hyperthyroidism.
Diarrhea should also be differentiated from fecal incontinence, which is the involuntary release of rectal contents. Incontinence is more common when the stool is liquid than when it is solid and reflects abnormal functioning of the anorectal or pelvic muscle. Diarrhea is considered acute when it lasts up to 7-14 days and chronic when it lasts over 2-3 weeks.
Let's move on to acute diarrhea! The most common causes of acute diarrhea are infectious agents. In this case, not to mention the infectious agents and their "way" of acting, they have physiopathological mechanisms represented by: 1. production of toxins (preformed toxin, endotoxin and cytotoxin), 2. enteroadherence, 3. invasion of the mucosa (which may be minimal, variable or severe) and 4. systemic infection.
Acute diarrhea can also be caused by ingested medicines or toxins, chemotherapy, resumption of enteral feeding after prolonged fasting, after blockage of feces (overflow diarrhea) or in particular situations, such as marathon race. In addition, acute diarrhea may represent the onset of chronic diarrheal disease.
Infectious diarrhea is responsible for more than 5-8 million deaths annually in children under 5 years of age, especially in developing countries where acute infectious diarrhea is a major cause of protein-calorie malnutrition and dehydration. favourable factors include poor water sanitation and supply, lack of refrigeration, overpopulation and lack of personal hygiene, poverty, lack of access to health services and lack of education.
Even in advanced countries such as the US, significant economic losses are "attracted" to acute infectious diarrhea that is responsible for 250,000 hospitalizations and nearly 8 million outpatient medical consultations annually. Most infectious diarrheals are acquired through fecal-oral transmission through water or food contaminated with human waste as a result of inadequate sewage systems or through feces of wild or domesticated animals in inadequately filtered water. Beef, pork or poultry can be a source of infection when prepared inappropriately.
The surfaces on which food is prepared may be contaminated by microorganisms that are transmitted to uncooked food. Person-to-person transmission can also occur through aerosolization (Norwalk agent, rotaviruses), contamination of hands (Clostridium difficile) or surfaces, or, including, through sexual activity. Particularly high risk groups for acute infectious diarrhoea also include tourists, people who ingest shellfish, gay men (homosexual bowel syndrome), prostitutes and intravenous drug users. People with AIDS in particular are at risk for a lot of serious enteric infections.
Among children who attend daycare centers, acute infectious diarrhea usually results from person-to-person transmission. The most common pathogens involved in diarrhoea epidemics in daytime care centres are Shigella, Giardia lamblia and Cryptosporidium. The secondary epidemic rate between 20-30% is an important source of infections for parents and siblings. Other institutions at high risk for the outbreak of acute infectious diarrhoea include institutes of care for the mentally and developmentally disabled, sanatoriums and hospitals.
I will complete this post with a few presentations about clinical features. Patients with acute infectious diarrhoea usually present with nausea, vomiting, abdominal pain, fever and diarrhoea, which may be watery, malabsorbent or bloody, depending on the specific pathogen. Patients who have ingested toxins or those with toxicogenic infection usually have nausea and vomiting as the main symptoms, but rarely high fever. Abdominal pain is mild, diffuse and colicative and comes from large volumes of secreted fluid that stimulates peristaltic and causes watery diarrhea.
Vomiting that begins a few hours after ingestion of a food suggests food poisoning due to a preformed toxin. Parasites that do not invade the intestinal mucosa, such as Giardia Lamblia and Cryptosporidium, usually cause only mild abdominal embarrassment. Giardia can also be associated with mild steatorea, meteorism and bloating. Invasive bacteria such as Campylobacter, Salmonella and Shigella, and cytotoxin agents such as Clostridium difficile and Escherichia Coli enterohemorrhagic, cause severe intestinal inflammation, abdominal pain and often high fever (sometimes peritoneal signs may suggest an acute abdomen).
Yersinia often infects the terminal ileum and the check and presents pain in the right iliac fossa and evocative sensitivity of acute appendicitis. Watery diarrhea is characteristic for microorganisms that invade the intestinal epithelium with minimal inflammation, such as enteric viruses, or microorganisms that adhere to but do not destroy the epithelium, such as enteropathogenic or enteroaderent E. coli, protozoa and helminths. Some microorganisms, such as Campylobacter, Aeromonas, Shigella and Vibrio, produce enterotoxins and invade the intestinal mucosa (patients therefore often present with watery diarrhea, followed within hours or days by bloody diarrhea).
The presence of systemic symptoms may provide additional clues to the underlying cause of diarrhea. Both shigelosis and enterohemorrhagic E. coli infection may be accompanied by hemolytic-uremic syndrome, especially in people who are very young or very elderly. Yersinia infection and occasionally other enteric bacterial infections may be accompanied by Reiter syndrome (arthritis, urethritis and conjunctivitis), thyroiditis, pericarditis or glomerulonephritis.
We continue the topic on June 20, addressing the differential diagnosis of acute diarrhea...
Let's hear it for good!
Dorin, Merticaru