|Solutions for Digestive Disorders|
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Motility of the Digestive Tract (DT)
The Digestive Tract (DT) is muscular and contracts rhythmically to conduct food through its length (peristalsis). The timing, strength, and coordination of muscular contraction is influenced by the composition of food and by state-specific body-brain conditions. If the contractions are too vigorous, crampy pain is experienced. If the contractions are too frequent, diarrhea results. Constipation occurs when contractions are sluggish and slow, or if sustained contractions act to obstruct the tube.
Disorders of peristalsis are referred to as "Motility Disorders." Medical diagnoses sometimes refer to motility disorders as if they were the cause of symptoms. With a few exceptions, motility problems are not causes but they are effects of food-DT interaction and DT-brain interactions.
The stomach stores and mixes ingested food, regulating the rate of transfer into the duodenum. Pacemaker cells of Cajal (ICCs) are located in the greater curvature that send activation signals in circumferential and longitudinal directions. Spike waves occur when the slow wave reaches a threshold and produce contractions. In guinea pig gastric smooth muscle, protein kinase C modulates the contraction frequency and the intracellular calcium concentration modulates the amplitude. Calcium is released in response to increased metabolic activity of the mitochondria.
The stomach and duodenum signal each other via release of neurotransmitters and hormones. Distension of the gastric antrum causes relaxation of the pylorus (antro-sphincteric reflex) and duodenum (antro-duodenal reflex). Distension of the duodenum causes antral relaxation (duodeno-antral reflex). Distension of the pyloric sphincter causes antral contraction (sphinctero-antral reflex). These reflexes facilitate the transport of gastric contents into the duodenum.
Every medical student learns that there is a dense arborization of signal pathways linking the brain with almost every body cell. This autonomic nervous system is the main driver and regulator of digestive tract functions. The sympathetic part of the autonomic system is the fight or flight arousal system that prepares the body for action. Digestive functions are shut down by sympathetic nervous system activity. Fight and flight arousal requires increased blood flow to muscles and decreased flow to the digestive tract. Secretions and motility are decreased. The fear response may trigger vomiting and defecation to empty the digestive tract in preparation for fleeing. People exposed often to threatening circumstances will experience digestive tract malfunctions from functional dyspepsia and gastroparesis to ulcers and inflammatory disorders in the small and large intestines.
The parasympathetic part of the autonomic system is concerned with processing food, resting, and restoration. The parasympathetic system uses acetylcholine as the transmitter and is found everywhere in the body, sending signals to muscle cells to contract. In the brain, acetylcholine has arousal functions in the right amounts but tends to cause depression in overdose.
Many common digestive tract symptoms are generated by over active acetylcholine mechanisms, especially nausea, vomiting, belching, cramps, defecation, sweating and runny nose. Nicotine mimics some of the actions of acetylcholine and even veteran smokers who chew nicotine gums for the first time may get these effects.
Drugs that block acetylcholine activity are popular in medicine and have many uses. Atropine is the prototype and along with related compounds has been used in medicines to treat upset digestive function. Atropinic drugs reduce secretions and block crampy abdominal pain from vigorous contractions of intestinal smooth muscle. Too much atropine and you are dry-mouthed, constipated and have trouble urinating; you may also have trouble thinking and remembering. Motility disorders are often caused by drugs that block acetylcholine activity such as antidepressants and antihistamines.
FD, Motility Disorders Management
Here are the basic principles:
Digestive disorders are common diseases that originate in the food supply. Diet revision should be primary therapy. The solution is to adjust the incoming food supply until the problem is resolved.
The gastrointestinal tract is a sensing, reactive device which monitors the material flowing through it. Symptoms arising from this system provide information about its dysfunction.
Seven basic symptoms alert the patient to gastrointestinal tract displeasure with food choices - nausea, heartburn, vomiting, bloating, pain, constipation and diarrhea.
In the stomach, a surface reaction results in upper-middle abdominal pain and nausea; sometimes vomiting is triggered. These are defensive responses that reject the offending food. Vomiting usually relieves pain and other discomforts. Some people induce vomiting to avoid discomforts after eating.
Recurrent irritation in the upper DT is food-caused until proven otherwise. Obviously smoking, drinking alcoholic beverages, coffee and teas are the first problems to eliminate, but surface "allergy" to common, "normal" foods may also be responsible. Symptoms from the upper digestive tract are often associated with lower abdominal pain, bloating, constipation and diarrhea. A trial of diet revision can provide prompt relief. If food holiday is unsuccessful, further investigation is always required.
Stomach Problems & Gastroparesis
Gastroparesis means stomach paralysis. The term refers to a variety of disorders characterized by delayed gastric emptying in the absence of obstruction. Problems in the stomach may be part of a more general food reactive, motility disorder. Recall that pacemaker cells of Cajal (ICCs), located in the greater curvature of stomach, send activation signals that produce produce contractions. A complex of interacting signals regulates stomach contraction and emptying. There is ample opportunity for things to go wrong. The first and most prevalent cause of motility disorders is eating too much of the wrong food. The definition of wrong is both general and highly individual.
In addition, many diseases interfere with stomach motility. Sanjeevi stated: "Abnormal gastrointestinal motility is seen in a third of diabetic patients as well as in patients with chronic neurological and rheumatological conditions, renal failure, and cirrhosis. The causes include disturbances in the functioning of vagal neurons, enteric neurons, ICCs, smooth muscle cells, or humoral factors. Genetic factors also contribute since gastric dysmotility occurs predominantly in females. Recently, it was shown that healthy female rats exhibit increased gastric neural nitric oxide synthase (nNOS) expression whereas diabetic female, but not male, rats exhibit significantly decreased nNOS expression as well as impaired relaxation. ICCs express KIT protein or CD117, a transmembrane receptor with tyrosine kinase activity. Immunostaining of full thickness antral biopsies obtained from 14 medically refractory gastroparetic patients undergoing placement of a gastric electrical stimulator showed absence of ICCs in one-third of the patients. Measurement of the emptying of solids is more sensitive for detection of gastroparesis than liquids. Solid emptying exhibits a lag phase followed by a prolonged linear emptying phase. Unexpectedly, the prime abnormality in patients with dyspepsia and autonomic dysfunction appears to be rapid gastric emptying. Accelerated early phase emptying may lead to delayed late phase emptying due to feedback inhibition by the duodeno-antral reflex."
Drugs for Motility Disorders
Drugs used in the attempt to improve gut motility (without adequate diet revision!) have a dismal record of doing harm with little or no benefit. In his review, Sanjeevi summarized the main disappointments: Metoclopramide may induce anxiety, tremors, dystonia, Parkinson's like symptoms, and depression. Erythromycin has a narrow therapeutic window, disrupts the bacterial flora, promotes antimicrobial resistance, and may induce cardiac arrythmias. Cisapride has been severely restricted due to risk for prolongation of the cardiac QT interval. Tegaserod has recently been withdrawn from the United States market due to cardiovascular side effects. A recent trial found that tegaserod had no significant effects on gastric motor, sensory, or myoelectric function in healthy volunteers using the SPECT technique. The earlier developed motilin receptor agonist, ABT-229, failed to show significant efficacy in relieving symptoms in patients with gastroparesis or functional dyspepsia. A newer motilin agonist, mitemcinal, produced a better response rate than placebo in symptomatic diabetic patients with body mass index <35 kg/m2 and hemoglobin A1c <10%. Subanalysis suggested that the improvement was more impressive in patients with nondelayed gastric emptying. Itopride, a dopamine (D2) antagonist, in US studies did not demonstrate a significant effect on the symptoms of upper abdominal pain and fullness or the Patient Global Assessment questionnaire in patients with functional dyspepsia.
Two agents show some promise: Domperidone, a dopamine 2 antagonist improves gastrointestinal transit. `Domperidone minimally crosses the blood-brain barrier and has few, if any, central nervous system side effects. Domperidone is available in 58 countries, but only through an investigation drug program in the United States for patients with medically refractory gastroparesis.
Ghrelin, a peptide present in gastric mucosa and neurons, enhances gastric emptying and accelerates fasting motility. In idiopathic gastroparesis, administration of ghrelin enhanced gastric emptying and improved meal-related symptoms suggesting a potential for ghrelin receptor agonists in the treatment of gastroparesis.
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