question: How do conditions like irritable bowel syndrome and inflammatory bowel disease cause pain if the intestine doesn't have pain receptors?
comment: The bowel has nerves which are stretch receptors. Stimulating those creates a "pain" interpretation in the brain, which is why gas in the gut can be very "painful." IBS and IBD conditions produce gases in the intestines which cause distention, which stimulates stretch receptors, which the brain perceives as pain.
passages: Full body or localized pain to the extremities (known as acroparesthesia) or gastrointestinal (GI) tract is common in patients with Fabry disease. This acroparesthesia is believed to be related to the damage of peripheral nerve fibers that transmit pain. GI tract pain is likely caused by accumulation of lipids in the small vasculature of the GI tract which obstructs blood flow and causes pain.
  
  Section::::Signs and symptoms.:Kidney.
   Each subsection of the gut has an associated visceral afferent nerve that transmits sensory information from the viscera to the spinal cord, traveling with the autonomic sympathetic nerves. The visceral sensory information from the gut traveling to the spinal cord, termed the visceral afferent, is non-specific and overlaps with the somatic afferent nerves, which are very specific. Therefore, visceral afferent information traveling to the spinal cord can present in the distribution of the somatic afferent nerve; this is why appendicitis initially presents with T10 periumbilical pain when it first begins and becomes T12 pain as the abdominal wall peritoneum (which is rich with somatic afferent nerves) is involved.
   General visceral afferent sensations are mostly unconscious visceral motor reflex sensations from hollow organs and glands that are transmitted to the CNS. While the unconscious reflex arcs normally are undetectable, in certain instances they may send pain sensations to the CNS masked as referred pain. If the peritoneal cavity becomes inflamed or if the bowel is suddenly distended, the body will interpret the afferent pain stimulus as somatic in origin. This pain is usually non-localized. The pain is also usually referred to dermatomes that are at the same spinal nerve level as the visceral afferent synapse.
  
  Section::::Function.:Vascular effects.
   BULLET::::- the pain must be located in the upper part of the abdomen and/or the right upper quadrant of the abdomen
  
  BULLET::::- episodes of pain must last at least 30 minutes
  
  BULLET::::- the symptoms must be recurrent, and occur at differing intervals
  
  BULLET::::- the pain must incrementally increase to a "steady level"
  
  BULLET::::- the pain must be severe enough the patient's daily activities are affected, or that the patient must attend the emergency department
  
  BULLET::::- the pain must not be relieved by any of bowel movements, change in posture, or antacids; and,
   In 2005 New Scientist published a joint study by Bristol University and the University of Bath on the apparent healing power of cannabis on IBD. Reports that cannabis eased IBD symptoms indicated the possible existence of cannabinoid receptors in the intestinal lining, which respond to molecules in the plant-derived chemicals. CB1 cannabinoid receptors – which are known to be present in the brain – exist in the endothelial cells which line the gut, it is thought that they are involved in repairing the lining of the gut when damaged.
   BULLET::::- Abnormal motility Studies have shown altered muscle contractility and tone, bowel compliance, and transit may contribute to many of the gastrointestinal symptoms of FGID which may include diarrhea, constipation, and vomiting.
  
  BULLET::::- Visceral hypersensitivity In FGID there is poor association of pain with GI motility in many functional GI disorders. These patient often have a lower pain threshold with balloon distension of the bowel (visceral hyperalgesia), or they have increased sensitivity even to normal intestinal function; Visceral hypersensitivity may be amplified in patients with FGIDs.
   The two types differ only in the nature of the inciting event. Type I CRPS develops following an initiating noxious event that may or may not have been traumatic, while type II CRPS develops after a nerve injury.
   Functional gastrointestinal disorders the most common of which is irritable bowel syndrome. Functional constipation and chronic functional abdominal pain are other functional disorders of the intestine that have physiological causes, but do not have identifiable structural, chemical, or infectious pathologies.
  
  Section::::Clinical significance.:Symptoms.
  
  Several symptoms are used to indicate problems with the gastrointestinal tract:
  
  BULLET::::- Vomiting, which may include regurgitation of food or the vomiting of blood
  
  BULLET::::- Diarrhea, or the passage of liquid or more frequent stools
  
  BULLET::::- Constipation, which refers to the passage of fewer and hardened stools
   Mouse studies have suggested some symptoms of Crohn's disease, ulcerative colitis, and irritable bowel syndrome have the same underlying cause. Biopsy samples taken from the colons of all three patient groups were found to produce elevated levels of a serine protease. Experimental introduction of the serine protease into mice has been found to produce widespread pain associated with irritable bowel syndrome, as well as colitis, which is associated with all three diseases. Regional and temporal variations in those illnesses follow those associated with infection with the protozoan "Blastocystis".
   BULLET::::1. The presence of an initiating noxious event or a cause of immobilization
  
  BULLET::::2. Continuing pain, allodynia (perception of pain from a nonpainful stimulus), or hyperalgesia (an exaggerated sense of pain) disproportionate to the inciting event
  
  BULLET::::3. Evidence at some time of edema, changes in skin blood flow, or abnormal sudomotor activity in the area of pain
  
  BULLET::::4. The diagnosis is excluded by the existence of any condition that would otherwise account for the degree of pain and dysfunction.
  
  According to the IASP, CRPS II (causalgia) is diagnosed as follows:
   The timing of the symptoms in relation to the meal may differentiate between gastric and duodenal ulcers: A gastric ulcer would give epigastric pain during the meal, associated with nausea and vomiting, as gastric acid production is increased as food enters the stomach. Pain in duodenal ulcers would be aggravated by hunger, relieved by a meal, and is associated with night pain.
   Section::::Mechanism.
  
  There are different types of neurons involved in innervating the lower GI tract these include: the enteric nervous system; located within the wall of the gut, and the extrinsic nervous system; comprising sympathetic and parasympathetic innervation. The enteric nervous system directly controls the gut motility, whereas, the extrinsic nerve pathways influence gut contractility indirectly through modifying this enteric innervation. In almost all cases of neurogenic bowel dysfunction it is the extrinsic nervous supply affected and the enteric nervous supply remains intact. The only exception being Parkinson's disease, as this can affect both the enteric and extrinsic innervation.
   So, biliary dyskinesia is a dynamically (functional...not fixed mechanical) obstructive, pain-producing disorder. Obstruction by a stone or tumor is a static, mechanical obstruction and tends to produce a more intense pain known as biliary colic.
  
  Failure of the biliary sphincter of Oddi can be distinguished from failure of the pancreatic sphincter.
  
  Section::::Diagnosis.
   Previous studies have shown that CB1 receptors located on the nerve cells in the gut respond to cannabinoids by slowing gut motility, therefore reducing the painful muscle contractions associated with diarrhea. CB2, another cannabinoid receptor predominantly expressed by immune cells, was detected in the gut of IBD sufferers at a higher concentration. These receptors, which also respond to chemicals in cannabis, appear to be associated with apoptosis – programmed cell death – and may have a role in suppressing the overactive immune system and reducing inflammation by mopping up excess cells.
   The main symptom of enteric neuropathy is severe and constant pain. Other symptoms include nausea, vomiting, diarrhoea, constipation, bloating and abdominal abnormalities. In addition malabsorption and poor nutrition are common, as the digestive system begins to fail. Symptom management is very important and the main priority is usually to get on top of the pain. However, as most people may have been waiting for years for a diagnosis they are often already addicted to painkillers (such as tramadol and oramorph) and these have adverse effects on the primary condition.
  
  Section::::Diagnosis.
   Medication-related dyspepsia is usually related to NSAIDs and can be complicated by bleeding or ulceration with perforation of stomach wall.
  
  Section::::Treatment.
  
  Functional and undifferentiated dyspepsia have similar treatments. Drug therapy decisions are difficult because trials included heartburn in the definition of dyspepsia. This led to the results favoring proton pump inhibitors (PPIs), which are effective for the treatment of heartburn.
   SCN5A mutations are found in a small number of people who have IBS, particularly the constipation-predominant variant (IBS-C). The resulting defect leads to disruption in bowel function, by affecting the Nav1.5 channel, in smooth muscle of the colon and pacemaker cells.
  
  Section::::Mechanism.
  
  Genetic, environmental, and psychological factors seem to be important in the development of IBS. Studies have shown that IBS has a genetic component even though there is a predominant influence of environmental factors.
   BULLET::::- Inflammatory bowel disease: IBS may be a type of low-grade inflammatory bowel disease. Researchers have suggested IBS and IBD are interrelated diseases, noting that people with IBD experience IBS-like symptoms when their IBD is in remission. A three-year study found that patients diagnosed with IBS were 16.3 times more likely to be diagnosed with IBD during the study period. Serum markers associated with inflammation have also been found in patients with IBS.
   There is evidence that abnormalities occur in the gut flora of individuals who have IBS, such as reduced diversity, a decrease in bacteria belonging to the phylum "Bacteroidetes", and an increase in those belonging to the phylum "Firmicutes". The changes in gut flora are most profound in individuals who have diarrhoea predominant IBS. Antibodies against common components (namely flagellin) of the commensal gut flora are a common occurrence in IBS affected individuals.
   There is compelling evidence that the N-methyl-D-aspartate (NMDA) receptor has significant involvement in the CNS sensitization process. It is also hypothesized that elevated CNS glutamate levels promote wind-up and CNS sensitization. In addition, there exists experimental evidence demonstrating the presence of NMDA receptors in peripheral nerves. Because immunological functions can modulate CNS physiology, it has also been hypothesized that a variety of immune processes may contribute to the initial development and maintenance of peripheral and central sensitization. Furthermore, trauma related cytokine release, exaggerated neurogenic inflammation, sympathetic afferent coupling, adrenoreceptor pathology, glial cell activation, cortical reorganisation, and oxidative damage (e.g., by free radicals) are all factors which have been implicated in the pathophysiology of CRPS.
   Section::::Diagnosis.
   Early symptoms can include periodic abdominal pain, nausea, vomiting (sometimes green in color from bile), pulling legs to the chest area, and intermittent moderate to severe cramping abdominal pain. Pain is intermittent—not because the intussusception temporarily resolves, but because the intussuscepted bowel segment transiently stops contracting. Later signs include rectal bleeding, often with "red currant jelly" stool (stool mixed with blood and mucus), and lethargy. Physical examination may reveal a "sausage-shaped" mass, felt upon palpating the abdomen. Children, or those unable to communicate symptoms verbally, may cry, draw their knees up to their chest, or experience dyspnea (difficult or painful breathing) with paroxysms of pain.
   Section::::Diagnosis.
  
  Diagnosis is primarily based on history as specific IgE and skin prick tests are typically negative and the exclusion of other disorders that present similar clinical features, such as infectious gastroenteritis, celiac disease, inflammatory bowel disease, and eosinophilic gastroenteritis, among others.
  
  Section::::Treatment.
   The intestinal wall is also affected. In humans there is a thickening of the intestinal wall (ileum, appendix and caecum). In rats with heavy infestations there is a yellow discolouring of the surface of the intestinal walls.
  
  Section::::Clinical signs and diagnosis.
  
  BULLET::::- Abdominal pain which presents as a palpable mass on clinical examination
  
  BULLET::::- Anorexia
  
  BULLET::::- Diarrhoea
  
  BULLET::::- Vomiting
   In large bowel obstruction, the pain is felt lower in the abdomen and the spasms last longer. Constipation occurs earlier and vomiting may be less prominent. Proximal obstruction of the large bowel may present as small bowel obstruction.
  
  Section::::Causes.
  
  Section::::Causes.:Small bowel obstruction.
  
  Causes of small bowel obstruction include:
  
  BULLET::::- Adhesions from previous abdominal surgery (most common cause)
  
  BULLET::::- Barbed sutures
  
  BULLET::::- Pseudoobstruction
  
  BULLET::::- Hernias containing bowel
  
  BULLET::::- Crohn's disease causing adhesions or inflammatory strictures
  
  BULLET::::- Neoplasms, benign or malignant
  
  BULLET::::- Intussusception
  
  BULLET::::- Volvulus
  
presuppositions: Pain can only be felt if there is pain receptor.
corrections: Pain can be felt from stretch receptor.
raw_presuppositions: Pain is felt in the intestines. Intestine doesn't have pain receptor. Pain can only be felt if there is pain receptor.
raw_corrections: Pain is not felt in the intestines, but the brain interprets stimulation to stretch receptors as pain. The bowel has stretch receptos which when stimulated cause pain. Pain can be felt from stretch receptor.