Intestinal peristalsis physiology and motility disorders

Physiology of intestinal peristalsis with pathophysiology of various motility disorders.

1. INTESTINAL PERISTALSIS PHYSIOLOGY AND MOTILITY DISORDERS Dr. Subhasish Deb Burdwan Medical College Dept of General Medicine Dr Subhasish Deb, BMCH

2. GIT PHYSIOLOGY Smooth muscles of GIT made of many muscle bundles Outer= LONGITUDINAL Inner= CIRCULAR Dr Subhasish Deb, BMCH

3. Smooth muscles of a bundle connected with GAP JUNCTIONS Adjacent bundles also connected with GAP Junctions Stimulation of 1 bundle stiml the other bundle thus acts as an electrical syncitium Dr Subhasish Deb, BMCH

4. ELECTRICAL Activity of git Interstitial cells of CAJAL Present between long and circular layer Can produce pacemaker activity (like heart) Electrical activity spreads via gap junctons Interstitial cell of cajal Dr Subhasish Deb, BMCH

5. Electrical activity in one smooth muscle The RMP is fluctuating between -65 to -45mV This Basic Electrical Rhythm(BER) is initiated by interstitial cells of Cajal BER aka Slow Waves Dr Subhasish Deb, BMCH

6. Ca channels present allow Ca 2+ to enter continuously This raises the RMP from -65 to -45 when K + channels open Efflux of K and the RMP comes back to -65mV These are NOT ACTION POTENTIALS They do NOT CAUSE CONTRACTIONS RATE OF SLOW WAVES: Stomatch : 3/min Duodenum : 12/min Jejunum, ileum : 9/min Dr Subhasish Deb, BMCH

7. So excitibility of GIT soomth muscles increases progressively and decr progressively IF peak of this wave touches the threshhold potential -40mV, voltage sensitive Ca channles open –- Ca influx –- Contraction When repolarisation occurs, it still finds the slow wave above the threshhold so another spike is produced These Aps at the top are called SPIKE POTENTIALS Dr Subhasish Deb, BMCH

8. Key Points: Action potentials = Spike potential How many spikes(Aps) produced depends on how long the slow wave remains above TP If slow wave does not reach TP then no APs Dr Subhasish Deb, BMCH

9. Muscle excitability can ne changed by change in RMP. RMP to -50mV = more excitability (slow waves will be frequently over TP, more spikes) RMP to -70mV = less excitability Factors inc RMP: Muscle Stretch : more Ca influx through channels Acetylcholine : vagus Parasympathetic stimulation Some hormones Factors decr RMP: Nor epinephrine Sympathetic stimulation Dr Subhasish Deb, BMCH

10. Nervous control of GIT ENTERIC NERVOUS SYSTEM Can work independent of higher impulses (thus also called mini brain) Considered as 3 rd part of ANS Consists of 2 neuronal layers Myentric plexus ( Aurbach’s plexus) in muscular layer Missner’s plexus in submucosa Dr Subhasish Deb, BMCH

11. Dr Subhasish Deb, BMCH

12. Missner’s plexus Submucosal Mainly regulates secretion from mucosal & submucosal glands Blood flow in these layers determine absorption Aurbach’s plexus In Muscular layer Mainly concerned with motility Dr Subhasish Deb, BMCH

13. Stimulus for peristalsis: Stretch by food bolus – stimulates sensory neurons which then stimulate myenteric plexus Chemical signals or irritation of mucosa Peristalsis: for it to occur, the oral side of the GIT to the food bolus should contract and the anal side should relax Dr Subhasish Deb, BMCH

14. The myenteric plexus has 2 sets of neurons: Ascending (signal moves towards oral side) Descending (signal moves towards anal side) When sensory system (stretch) stimuates ascending fibres , they release Ach & Sub P which are positive neuro transmitters – go on stimulating fibres towards oral side Contraction of muscles behind the food bolus Dr Subhasish Deb, BMCH

15. At the same time sensory neurons also stimulate the descending neurons. They release NO and Vaso Inhibitory Peptide(VIP) This causes relaxation of smooth muscle distal to the food bolus Food particle moves forward, causes local stretch in the new area ad the whole thing repeats. Dr Subhasish Deb, BMCH

16. Ach Sub P NO VIP Aurbach’s plexus Stomach Missner’s plexus Intestine Vagus Sensory nerve Dr Subhasish Deb, BMCH

17. Parasympathetic control: (directly innervaye neurons of both the plexus thus the myenteric & missner’s plx can be considered as post ganglionic fibres of para sys) Inc motility Inc digestion Inc absorbtion Sympathetic control: via postganglionic fibre Dec motility Dec digestion Dec absorbtion (directly affect splanchnic vessels- vasoconstriction- diverts blood to other areas) Dr Subhasish Deb, BMCH

18. REFLEXES Intra gut reflex: Local reflex Local irritaton /dilatation – inc secretion, contraction Ganglionic reflex: Gastrocolic Enterogastric Coloileal Cns reflex: Vago vagal reflex ( senry input from stomach to medulla via vagus and back to stomach via vagus ) Defecation reflex Dr Subhasish Deb, BMCH

19. Motility disorders of intestine Esophagus : Achalasia, GERD Stomach : Gastroparesis Small intestine : Ileus Colon : Hirschsprung disease Dr Subhasish Deb, BMCH

20. Achalasia Achalasia is a primary esophageal motility disorder characterized by the absence of esophageal peristalsis and impaired relaxation of the lower esophageal sphincter (LES) in response to swallowing. Signs and Symptoms: Dysphagia (m/c) Regurgitation Chest pain Weight loss Physical exam and lab studies are non contributary Dr Subhasish Deb, BMCH

21. Pathophysiology: LES pressure and relaxation are regulated by excitatory ( eg , acetylcholine, substance P) and inhibitory ( eg , nitric oxide, vasoactive intestinal peptide) neurotransmitters. Here there is lack of inhibitory neurotransmission. Dr Subhasish Deb, BMCH

22. Barium Swallow shows Bird’s Beak appearance Dr Subhasish Deb, BMCH

23. Other investigations: Esophageal manometry : incomplete LES relaxation on swallowing High LES resting pressure Absent esophageal peristalsis Prolonged esophageal pH moitoring : To rule out GERD Esophageogastroduodenoscopy To rule out CA of GEJ and fundus Dr Subhasish Deb, BMCH

24. Treatment: Pharmacological: Ca channel blockers, nitrates – for elderly pts who cannot undergo pnuemaic dilatation or surgery E ndoscopic intrasphincteric injection of botulinum toxin to block acetylcholine release at the level of the LES Surgical: Laparoscopic Heller myotomy , preferably with anterior ( Dor ; more common) or posterior ( Toupet ) partial fundoplication Peroral endoscopic myotomy (POEM) Dr Subhasish Deb, BMCH

25. Dr Subhasish Deb, BMCH

26. gerd Gastroesophageal reflux disease occurs when the amount of gastric juice that refluxes into the esophagus exceeds the normal limit, causing symptoms with or without associated esophageal mucosal injury ( ie , esophagitis ) Dr Subhasish Deb, BMCH

27. Signs and Symptoms: (typical esophageal) Heart burn Regurgitation Dysphagia (Atypical extraesophageal symptoms) Coughing and/or wheezing Hoarseness, sore throat Otitis media Noncardiac chest pain Enamel erosion or other dental manifestations Dr Subhasish Deb, BMCH

28. Investigations: Upper GI endoscopy Esophageal manometry Ambulatory 24-hour pH monitoring: Criterion standard in establishing a diagnosis of gastroesophageal reflux disease Management principles: Control symptoms Heal esophagitis Prevent recurrent esophagitis and complications Dr Subhasish Deb, BMCH

29. Management: Life style modification- Losing weight (if overweight) Avoiding alcohol, chocolate, citrus juice and tomato-based products Avoiding peppermint, coffee and possibly the onion family Eating small, frequent meals rather than large meals Waiting 3 hours after a meal to lie down Refraining from ingesting food (except liquids) within 3 hours of bedtime Elevating the head of the bed 8 inches Avoiding bending or stooping positions Dr Subhasish Deb, BMCH

30. Pharmacotherapy: H2 receptor antagonists ( eg , ranitidine, cimetidine, famotidine, nizatidine ) Proton pump inhibitors ( eg , omeprazole, lansoprazole , rabeprazole , esomeprazole, pantoprazole) Prokinetic agents ( eg , aluminum hydroxide) Antacids ( eg , aluminum hydroxide, magnesium hydroxide) Surgical options: Transthoracic and transabdominal fundoplications are performed for gastroesophageal reflux disease, including partial (anterior or posterior) and circumferential wraps Dr Subhasish Deb, BMCH

31. Indications of Fundoplication: Patients with symptoms that are not completely controlled by proton pump inhibitors Patients with well-controlled reflux disease who desire definitive, one-time treatment The presence of Barrett esophagus The presence of extraesophageal manifestations Young patients Poor patient compliance with regard to medications Postmenopausal women with osteoporosis Patients with cardiac conduction defects Cost of medical therapy Dr Subhasish Deb, BMCH

32. Gastroparesis Aka delayed gastric emptying paresis (partial paralysis) of the stomach, resulting in food remaining in the stomach for an abnormally long time May occur due to: Damage of vagus nerve Improper functioning of muscle of stomach Dr Subhasish Deb, BMCH

33. Signs and symptoms: Chronic nausea (93%) Vomiting (especially of undigested food) (68-84%) Abdominal pain (46-90%) A feeling of fullness after eating just a few bites (60-86 %) Causes: DM- autonomic neuropathy CTDs- scleroderma, E hler Danlos Parkinson’s disease Abdominal surgery- injury to vagus Idiopathic- autoimmune response triggered by viral inection Diagnosis: gastric emptying scan (radio nucleotide) Dr Subhasish Deb, BMCH

34. Treatment: Dietary changes Low fiber diet Avoid fat Smaller meals spaced 2-3 hrs apart Prokinetic medications Domperidone , cisapride , erythromycin, metochopramide Adjustment of insulin dose for DM Jejunostomy tube, parenteral nutrition Dr Subhasish Deb, BMCH

35. ileus hypomotility of the gastrointestinal tract in the absence of mechanical bowel obstruction Although certain older terms such as gallstone ileus and meconium ileus persist in usage, they are now misnomers. Pathophysiology: The exact pathogenesis of ileus remains unclear. Postoperative ileus may be mediated via activation of inhibitory spinal reflex arcs. Dr Subhasish Deb, BMCH

36. Although ileus has numerous causes, the postoperative state is the most common setting for the development of ileus. Physiologic ileus spontaneously resolves within 2-3 days, after sigmoid motility returns to normal. Ileus that persists for more than 3 days following surgery is termed postoperative adynamic ileus or paralytic ileus Dr Subhasish Deb, BMCH

37. Risk Factors: gastrointestinal surgery or other GI procedures electrolyte imbalance diabetic ketoacidosis ( DKA) and other causes of metabolic acidosis hypothyroidism medications (e.g. opiates or antimuscarinics ) severe illness (Inflammation with peritonitis) spinal cord injury, those with injury above thoracic vertebrae 5 (T5) will have hypomotility problems within the bowel Dr Subhasish Deb, BMCH

38. Treatment: NPM + nasogastic suction + parenteral nutrition (to avoid perforation) Bowel movements may be stimulated by lactulose, erythromycin. a systematic review of randomized controlled trials show that chewing gum, as a form of 'sham feeding', may stimulate gastrointestinal motility Correction of underlying cause (electrolytes, thyroid) Dr Subhasish Deb, BMCH

39. Hirschprung disease Hirschsprung disease is a developmental disorder characterized by absence of ganglia in the distal colon, resulting in a functional obstruction should be considered in any newborn that fails to pass meconium within 24-48 hours of birth Dr Subhasish Deb, BMCH

40. Pathophysiology: Normal motility is primarily under the control of intrinsic neurons. In the absence of extrinsic signals, bowel function remains adequate, owing to the complex reflexive architecture of the enteric nervous system (ENS ) Enteric ganglion cells are derived from the neural crest during embryonic development . One possible etiology of Hirschsprung disease is the arrest of aboral neuroblast migration. Dr Subhasish Deb, BMCH

41. Diagnosis: Definitive diagnosis is made by suction biopsy of the distally narrowed segment. A histologic examination of the tissue would show a lack of ganglionic nerve cells. Treatment: surgical removal (resection) of the abnormal section of the colon, followed by reanastomosis . Dr Subhasish Deb, BMCH

42. Swenson, Soave, Duhamel, and Boley procedures The pull-through procedure repairs the colon by connecting the functioning portion of the bowel to the anus. Dr Subhasish Deb, BMCH

43. THANK YOU Dr Subhasish Deb, BMCH