1. Propulsion and Mixing of Food in the Alimentary Tract
Chapter 63:
Propulsion and Mixing of Food in the Alimentary Tract

2. Motility Chewing and Swallowing Esophageal Motility Gastric Motility
Small Intestinal Motility
Large Intestinal Motility

3. Chewing (mastication)
Purpose of Chewing -
Breaks cells - breaks apart undigestible cellulose
Increases surface area - decreases particle size
Mixes food with saliva -
Begins digestion of starches (-amylase, lingual lipase)
Lubricates food for swallowing

4. Nervous Control of Chewing
Innervation -
5th cranial nerve innervates muscles of mastication
Controlled by nuclei in brain stem
Reflex mechanism -
Food in mouth  muscles of mastication relax  jaw drops  stretch reflex  rebound contraction  pushes food against lining of mouth  repeat

5. Swallowing (deglutination)
Three stages -
Voluntary - initiates swallowing process
Pharyngeal - passage of food through pharynx into esophagus
Esophageal - passage of food from pharnyx to
stomach

6. Pharyngeal Stage of Swallowing
Reflex controlled by brain stem -
1. Food in pharynx - tactile stimulation
2. Soft palate pulled upward
3. Palatopharyngeal folds (“sizer”) pulled together
4. Trachea is closed (respiration inhibited)
- Vocal cords approximated
- Larynx raises and epiglottis covers larynx
5. Relaxation of UES
6. Peristaltic contraction of pharnyx

7. Nervous Control of Swallowing
Swallowing Center - medulla
Sensory input from pharnyx and esophagus
Coordinates activity from vagal nuclei with other centers (e.g., inhibits respiratory center)
Pharyngeal Phase -
Food in pharynx  afferent sensory input via vagus / glossopharyngeal N.  swallowing center  brain stem nuclei  efferent input to pharynx.
Figure 63-1; Guyton & Hall

8. Esophageal Stage of Swallowing
Primary peristalsis - continuation of pharyngeal peristalsis
Secondary peristalsis -
Induced by distention
Repeats until bolus is cleared
Upper esophagus - upper 1/3 is striated muscle
Lower esophagus - lower 2/3 is SM

9. Nervous Control of Esophageal Phase
Primary peristalsis -
Continuation of pharyngeal peristalsis
Coordinated by swallowing center
Cannot occur after vagotomy (striated muscle)
Secondary peristalsis -
Stretch related afferent sensory input to ENS and swallowing center are both involved
Can occur after vagotomy (SM)

10. Esophageal Pressures Between Swallows During Swallowing
High pressure at sphincters
Pressure in esophageal body  intrapleural pressure
During Swallowing
UES relaxes - (low pressure)
Peristaltic wave - (high pressure)
LES and fundus relax - receptive relaxation (low pressure). Vagal input is inhibitory. VIP is transmitter for receptive relaxation.

11. Esophageal Sphincters - Purpose
Purpose of high resting pressures in UES and LES
UES - keeps air from entering esophagus
LES - prevents acid reflux into esophagus

12. Disorders of Swallowing (Dysphagia)
CVA (stroke) / cranial nerves damage
Aspiration - UES and pharyngeal contractions are not coordinated
Secondary peristalsis is still functional
Muscular diseases - myasthenia gravis, polio, botulism
Anesthesia - aspiration of stomach contents.

13. Gastroesophageal Reflux Disease (GERD)
Heartburn / acid indigestion (1/10 people)
Backwash of acid, pepsin, and bile into esophagus
Can lead to -
stricture of esophagus (scar tissue)
asthma (aspiration)
chronic sinus infection (reflux into throat)
Barrett’s esophagus

14. Achalasia and Megaesophagus
What is the cause / characteristics?
Motility disorder affecting lower 2/3 of esophagus
- LES fails to relax - LES pressure is high
- Organized peristaltic contractions are absent
Neurological problem with ENS (myenteric plexus)
After months/years
- megaesophagus develops can hold > 1 liter of food
Esophageal ulceration, rupture, and death can occur

15. Achalasia and Megaesophagus
What are the symptoms?
Difficulty swallowing liquids and solids
Regurgitation of undigested food
Weight loss, halitosis, excessive belching, heartburn

16. Achalasia and Megaesophagus
What is the treatment?
(1) Anti-spasmotic drugs that relax smooth muscle
(2) Pneumatic dilator (stiff balloon)
(3) Surgical myotomy

17. Gastric Motility Functions of gastric smooth muscle -
Relaxes to accommodate food - orad area
(receptive relaxation)
Mixes food with gastric juice - caudad area
(retropulsion)
Propels chyme into duodenum - caudad area
(antral pump)

18. Physiologic anatomy
of the stomach
Figure 63-2; Guyton & Hall

19. Motility of the Orad Area
Contractile activity - Low amplitude contractions occur as meal empties
Receptive relaxation - (VIP is neurotransmitter)
Vagovagal reflex - vagal aff. carry impulses to CNS - vagal eff. carry impulses from CNS to stomach
Vagotomy abolishes reflex
Gastric distensibility -
CCK increases (decreases gastric emptying)
Gastrin effect not physiologic

20. Motility of the Caudad Area
Peristalsis is the primary contractile event
Pressure tracings show -
Increased magnitude of contraction on approach to antrum
Decreased phase lag on approach to antrum
Decreased phase lag causes increased velocity of peristaltic wave

21. Electrical and Mechanical Events
Relationship between slow wave and muscle tension in caudad area -
Slow wave depolarization can elicit contraction of SM (without spikes) - stomach only
Slow wave plateau must reach threshold to cause SM contraction
Larger slow waves that have spike potentials cause increased strength of SM contraction

22. Regulation of Gastric Emptying
Chyme must enter duodenum at proper rate
pH must be optimal (high) for enzyme function
Slow enough for nutrient absorption
Immediately after meal - emptying does not occur before onset of gastric contractions
Conditions favor emptying -
(a) Increased tone of orad stomach
(b) Forceful peristaltic contractions
(c) Decreased tone of pylorus
(d) Absence of segmental contractions in intestine

23. Gastric Emptying is Accomplished by Coordinated Activities of Stomach,
Pylorus, and Small Intestine
Immediately after a meal
Conditions favor emptying
Intestinal receptors
activated

24. Regulation of Gastric Emptying
Activation of receptors in intestinal mucosa initiates enterogastric reflexes. This decreases gastric emptying by -
(a) Relaxation of orad stomach
(b) Decreased force of peristaltic contractions
(c) Segmentation contractions in intestine

25. Intestinal Receptors - Gastric Emptying
Intestinal mucosa receptors - stimulated by high or low osmolarity, acid, fat, and protein
Receptors trigger enterogastric reflexes
Fat/proteins - CCK release increases gastric distensibility which decreases gastric emptying
Acid - decreases gastric emptying (in 20-40s) via intrinsic neural reflex
Involvement of other hormones - probably not physiologic

26. Small Intestinal Motility
Small intestinal motility contributes to digestion and absorption by -
Mixing chyme - with digestive enzymes and other secretions
Circulation of chyme - to achieve optimal exposure to
mucosa
Propulsion of chyme - in an aboral direction

27. Small Intestinal Motility
Two types of movements in small intestine following a meal -
Peristalsis - a propulsive movement recall “Law of Gut.”
Segmentation - a mixing movement

28. Role of Slow Waves Contraction is controlled by slow wave activity -
Slow wave frequency- 12/min duodenum, 10 jejunum, 8 ileum
Contraction frequency - limited by slow wave frequency
Spike potentials necessary - Unlike stomach, contractions do not occur in absence of spike potentials

29. Slow Wave Frequencies Along Small Intestine
Slow waves measured at six points along small intestine -
Slow wave phase lag -
- promotes propagation of contractions (peristalsis)
Slow wave frequency -
- decreases at distal portions of small intestine
(5 and 6 are distal)

30. Migrating Motility Complexes (MMC)
Purpose - (housekeeping function). Sweeps undigested residue toward colon to maintain low bacterial counts in upper intestine.
Most coordinated, rapid peristalsis. Occurs between meals.
Characteristics -
Periods of intense peristaltic contractions
Takes ~90 min to go from stomach to colon
Mediated by motilin and ENS

31. Control of Small Intestinal Motility
Whether spike potentials and hence contractions occur depends upon neural and hormonal input -
Nervous factors - (PNS - stimulates / SNS - Inhibits)
Peristaltic reflex - (Law of the Gut) - Mediated by ENS.
Intestino-intestinal reflex - severe distention inhibits bowel. Extrinsic nerves.
Gastroileal reflex - Meal stimulates. Ileocecal sphincter relaxes, ileal peristalsis increases. (gastrin, CCK, extrinsic nerves, ??).

32. Control of Small Intestinal Motility
Whether spike potentials and hence contractions occur depends upon neural and hormonal input -
Hormonal factors -
Epinephrine - released from adrenals - inhibits motility
Motilin - mediates migratory motor complexes
Serotonin and prostaglandins - there are large quantities in small intestine that can stimulate motility
Other hormones. Gastrin, CCK, and insulin stimulate contractions. Secretin and glucagon inhibit contraction. The roles of these are uncertain.

33. Ileocecal Junction
Functions as a valve and a sphincter -
Valvular function -
- prevents backflow into small intestine mechanically
Sphincter function -
- regulates movement of ileal contents into large intestine. ENS and extrinsic nerves.

34. Emptying at the ileocecal valve
Figure 63-4; Guyton & Hall

35. Motility of Large Intestine
Functions of large intestine smooth muscle -
Mixes chyme –
enhances fluid / electrolyte absorption (haustral
contractions)
Propels fecal material -
(mass movements)

36. Absorptive and storage functions of the large intestine
Figure 63-5; Guyton & Hall

37. Musculature of Large Intestine
Longitudinal SM - 3 groups (teneae coli)
Circular SM - continuous to anus
Internal anal sphincter - a thickening of circular SM
External anal sphincter - striated muscle, surrounds internal anal sphincter
Haustra (haustrations) - not fixed, appear and
disappear

38. Innervation of Large Intestine
Myenteric plexus - concentrated beneath teneae
Parasympathetic input -
Vagus innervates proximal colon
Pelvic nerves (S2-S4 ) - distal colon, rectum / anus
Sympathetic input - T10-L2
CG and SMG - proximal colon
IMG - distal colon
Hypogastric plexus - rectum and anal canal
External anal sphincter - pudendal nerves

39. Haustral Contractions
Purpose - Mixing movements facilitate fluid and electrolyte absorption (minimal propulsion)
Structural and functional basis -
They appear and disappear every 30-60s
Require contraction of longitudinal and circular SM
Circular SM is concentrated in some areas

40. Mass Movements Propulsive movements (modified peristalsis)
Purpose - move feces to rectum / stimulate
defecation reflex
Distance - transverse colon to sigmoid colon or rectum
Occurrence -
After meals, series lasting min. (1-2 min each)
Reflexes - gastrocolic reflex (distention of stomach) - duodenocolic reflex (distention of duo)

41. Control of Defecation There are three levels of control -
Intrinsic reflex
Spinal cord reflex
Involvement of higher centers

42. Intrinsic Defecation Reflex
Intrinsic reflex mediated entirely by ENS is initiated when feces enters rectum via mass movements
Rectal distention initiates afferent signals that spread through myenteric plexus to descending and sigmoid colon, and rectum. This causes contractions that force feces toward anus.
Internal anal sphincter relaxes and if external anal sphincter is voluntarily relaxed, defecation occurs.

43. Defecation Reflex - Spinal Cord
Parasympathetic cord reflex greatly intensifies intrinsic reflex (but is not different qualitatively)
Rectal distention also initiates cord reflex. Afferent signals go to sacral cord and then back to descending and sigmoid colon, and rectum by way of parasympathetic fibers in pelvic nerves.
The lower neurons S2-S4 provide sensory and motor fibers for defecation reflex. They are intact when spinal cord is injured at higher levels.

44. Afferent and efferent pathways of the parasympathetic mechanism
for enhancing the defecation reflex
Figure 63-6; Guyton & Hall

45. Defecation Reflex - Higher Centers
Afferent signals entering spinal cord initiate other effects that require intact spinal cord.
deep breath, closure of glottis, and increased abdominal pressure
all work to move fecal contents downward
Spinal transection or injury can make defecation a difficult process
cord defecation reflex can be excited (either digitally or with enema)

46. Colon Motility Disorders
Paralysis of defecation reflexes in spinal cord injuries -
Destruction of conus medularis
(only intrinsic reflex is functional)
Destruction between conus medularis and brain
(intrinsic reflex and local cord reflex are functional)
Function of external anal sphincter?

47. List of Sphincters Upper esophageal sphincter (pharyngoesophageal)
Lower esophageal sphincter (gastroesophageal)
Pyloric sphincter (gastroduodenal)
Ileocecal valve / sphincter
Internal anal sphincter
External anal sphincter

48. List of Reflexes - gastric distention relaxes ileocecal sphincter
Peristaltic Reflex:
- stretch bowel, proximal contraction, distal relaxation
Enterogastric Reflex:
- from duodenum to regulate gastric emptying
Gastroileal Reflex (gastroenteric)
- gastric distention relaxes ileocecal sphincter

49. List of Reflexes (cont’d)
Intestino-intestinal Reflex:
- over-distention or injury of bowel segment causes entire bowel to relax
Gastro- and Duodenocolic Reflexes:
- distention of stomach / duodenum initiates mass movements
Defecation Reflex (rectosphincteric)
- rectal distention initiates defecation