Transcript Introduction to Physiology: The Cell and General Physiology

U N I T XII
Textbook of Medical Physiology, 11th Edition
Chapter 63:
Propulsion and Mixing of Food in the Alimentary Tract
GUYTON & HALL
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Motility
• Chewing and Swallowing
• Esophageal Motility
• Gastric Motility
• Small Intestinal Motility
• Large Intestinal Motility
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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
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Nervous Control of Chewing
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
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Swallowing (deglutination)
Three stages • Voluntary - initiates swallowing process
• Pharyngeal - passage of food through pharynx
into esophagus
• Esophageal - passage of food from pharnyx to
stomach
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Pharyngeal Stage of Swallowing
• Reflex controlled by brain stem 1.
2.
3.
4.
Food in pharynx - tactile stimulation
Soft palate pulled upward
Palatopharyngeal folds (“sizer”) pulled together
Trachea is closed (respiration inhibited)
- Vocal cords approximated
- Larynx raises and epiglottis covers larynx
5. Relaxation of UES
6. Peristaltic contraction of pharnyx
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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
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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
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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)
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Esophageal Pressures
• Between Swallows
- 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.
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Esophageal Sphincters - Purpose
• Purpose of high resting pressures in UES
and LES
- UES - keeps air from entering esophagus
- LES - prevents acid reflux into esophagus
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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.
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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
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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
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Achalasia and Megaesophagus
• What are the symptoms?
- Difficulty swallowing liquids and solids
- Regurgitation of undigested food
- Weight loss, halitosis, excessive belching, heartburn
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Achalasia and Megaesophagus
• What is the treatment?
(1) Anti-spasmotic drugs that relax smooth muscle
(2) Pneumatic dilator (stiff balloon)
(3) Surgical myotomy
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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)
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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
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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
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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
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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
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Gastric Emptying is Accomplished
by Coordinated Activities of Stomach,
Pylorus, and Small Intestine
Immediately
after a meal
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Conditions
favor emptying
Intestinal receptors
activated
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
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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
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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
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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
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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
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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)
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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
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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, ??).
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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.
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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.
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Emptying at the
ileocecal valve
Figure 63-4; Guyton & Hall
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Motility of Large Intestine
Functions of large intestine smooth muscle -
• Mixes chyme –
enhances fluid / electrolyte absorption (haustral
contractions)
• Propels fecal material (mass movements)
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Absorptive
and storage
functions of
the large
intestine
Figure 63-5; Guyton & Hall
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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
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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
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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
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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 10-30 min. (1-2 min each)
- Reflexes
- gastrocolic reflex (distention of stomach)
- duodenocolic reflex (distention of duo)
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Control of Defecation
• There are three levels of control - Intrinsic reflex
- Spinal cord reflex
- Involvement of higher centers
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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.
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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.
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Afferent and
efferent pathways
of the
parasympathetic
mechanism
for enhancing the
defecation reflex
Figure 63-6; Guyton & Hall
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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)
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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?
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List of Sphincters
• Upper esophageal sphincter
(pharyngoesophageal)
• Lower esophageal sphincter
(gastroesophageal)
• Pyloric sphincter (gastroduodenal)
• Ileocecal valve / sphincter
• Internal anal sphincter
• External anal sphincter
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List of Reflexes
• Peristaltic Reflex:
- stretch bowel, proximal contraction, distal relaxation
• Enterogastric Reflex:
- from duodenum to regulate gastric emptying
• Gastroileal Reflex (gastroenteric)
- gastric distention relaxes ileocecal sphincter
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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
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