reference: guyton & hall

1. Chapter 64
Propulsion
And
Mixing
of
Food in the Alimentary Tract
Dr. Misbah-ul-Qamar

2. Dr. Misbah-ul-Qamar

3. INGESTION OF FOOD
• It is principally determined by
– Hunger
– Appetite
• these 2 mechanisms are extremely important
– They determine the amount & type of food
ingested
– Maintain an adequate nutritional supply for body
Dr. Misbah-ul-Qamar

4. Hunger Vs Appetite
• Hunger:
Intrinsic desire for food
• Appetite:
Preference for a particular type of food
Dr. Misbah-ul-Qamar

5. Hunger associated effects
– Craving for food
– Rythmical contractions of stomach
– Restlessness causing the individual to seek food
Dr. Misbah-ul-Qamar

6. Control of food intake
• The hypothalamus contains hunger center
• There are several neuronal centers of
hypothalamus which participate in control of
food intake
– Lateral nuclei
– Paraventricular nuclei
– Dorsomedial nuclei
– Arcuate nuclei
Dr. Misbah-ul-Qamar

7. Control of food intake (cont’d)
• Lateral nuclei of hypothalamus serve as
feeding center
– Stimulation of this area causes the person to eat
voraciously (hyperphagia)
– Destruction of lateral hypothalamus causes lack of
desire for food
Dr. Misbah-ul-Qamar

8. Control of food intake (cont’d)
• Lesions of paraventricular nuclei often cause
excessive eating
• Lesions of dorsomedial nuclei usually depress
eating behaviour
• Arcuate nuclei receive signals by certain
hormones of GIT & adipose tissue to regulate
food intake
Dr. Misbah-ul-Qamar

9. Dr. Misbah-ul-Qamar

10. Control of food intake (cont’d)
• Feeding behaviour is influenced by
– Signals of sight, smell & taste from cerebral cortex
– Neural signals from GIT about stomach filling
– Chemical signals from nutrients in blood
– Signals from GI hormones
– Signals from hormones released by adipose tissue
• hypothalamic centers have high density of
receptors for neurotransmitters & hormones
• Hunger center operates by exciting the motor
drives to search for food
Dr. Misbah-ul-Qamar

11. Satiety
• It is the state of being fed to or beyond
capacity
• A satiety center is located in the ventromedial
nucleus (VPN) of hypothalamus
• It inhibits appetite even in the presence of
food
• The arcuate nucleus has various neurons
which project onto satiety center
Dr. Misbah-ul-Qamar

12. Mechanics of food ingestion
• Important mechanisms involved in food
ingestion are
– Mastication
– Swallowing
Dr. Misbah-ul-Qamar

13. Mastication (Chewing)
• Process in which food is cut and ground into
small pieces with help of teeth is called
mastication, It is caused by chewing reflex
• It is the first step in digestive process
• Number of chews that is optimal depends on
the food but usually ranges from 20-25.
• Edentulous patients are restricted to soft diet
and have considerable difficulty in eating dry
food
Dr. Misbah-ul-Qamar

14. Role of teeth & jaw in mastication
• Teeth are admirably designed for chewing
– Anterior teeth (Incisors) provide cutting action
– Posterior teeth (molars) provide grinding action
• Jaw muscle control the movement of teeth
• Force of mastication muscles
• All the jaw muscles working together can close the teeth with a force as
great as
– 55 pounds on incisors
– 200 pounds on molars
Dr. Misbah-ul-Qamar

15. Control of mastication
• Muscles of mastication are striated & under voluntary control but chewing
process is mostly reflex
• muscles are innervated by mandibular branches of Trigeminal nerve
• Chewing process is controlled by centers present in brain stem
• Stimulation of specific reticular areas in brain stem also cause rythmical
chewing movements
• Higher nervous control on chewing is exerted by:
– hypothalamus
– Amygdala
– Cerebral cortex areas near the sensory areas for taste & smell
Dr. Misbah-ul-Qamar

16. Mechanism of chewing- chewing reflex:
Bolus of food in mouth
Reflex inhibition of jaw muscles
Dropping of lower jaw
Stretch reflex of lower jaw muscles
Rebound contraction
Closure of teeth
Again compression of bolus against the lining of mouth
Inhibition of jaw muscles again
Dr. Misbah-ul-Qamar

17. Significance of chewing:
• Breaks indigestible cellulose coats of fruits & vegetables
• Increases the surface area for the action of digestive enzymes
• Mixes the food with saliva
• Makes swallowing easier
• Prevents excoriation of gastrointestinal tract
• Increases the ease with which food is emptied into small intestine from
stomach
• Helps to stimulate taste buds
Dr. Misbah-ul-Qamar

18. Formation of a bolus
• It is the combined function of mouth & teeth
– While chewing, food is moved around the mouth
by tongue & muscles of cheeks
– It is mixed with saliva & formed into a soft mass
(bolus) ready for swallowing
• Length of time that food remains in mouth
depends on consistency of food
Dr. Misbah-ul-Qamar

19. Swallowing (Deglutition)
• It is a complicated mechanism
• It occurs after the chewing is complete &
bolus has been formed
Dr. Misbah-ul-Qamar

20. Dr. Misbah-ul-Qamar

21. Role of pharynx in swallowing
• It subserves both respiration & swallowing
• It is converted into a tract for propulsion of
food for only a few seconds at a time
• It is specially important that respiration not be
compromised because of swallowing
Dr. Misbah-ul-Qamar

22. Stages of Swallowing
• Swallowing can be divided into three stages
(1) Voluntary stage:
Initiates the swallowing process
(2) Pharyngeal stage:
Involuntary phase that passes food through the pharynx into the
esophagus
(3) Esophageal stage
Involuntary phase that transports food from the pharynx to the stomach.
Dr. Misbah-ul-Qamar

23. Stages of swallowing
Dr. Misbah-ul-Qamar

24. Voluntary stage of swallowing:
• It is initiated when the bolus of food or liquid food is
voluntarily propelled to back of mouth by tongue
• The movement of tongue is upward & backward
against the palate
• Swallowing is initiated voluntarily, but once begun, it
cannot be stopped
Dr. Misbah-ul-Qamar

25. Pharyngeal stage
• It is a series of automatic pharyngeal muscle contractions
• a reflex act which is initiated by voluntary movement
• Bolus of food in posterior part of mouth & pharynx stimulate
epithelial swallowing receptors
• Location of swallowing receptors
• These lie in the most sensitive tactile area i.e., in a ring around the
pharyngeal opening
• Greatest sensitivity of these receptors is on the tonsillar pillars
Dr. Misbah-ul-Qamar

26. Nervous initiation of pharyngeal stage
• Afferent signals
Pass through sensory portions of Trigeminal &
Glossopharyngeal nerve to Nucleus Of Tractus
Solitarius and the Nucleus Ambiguus
• Efferent signals
From the control centers pass through
Trigeminal, Glossopharyngeal, Vagus and
Hypoglossal nerves to pharyngeal muscles
Dr. Misbah-ul-Qamar

27. Nervous control of swallowing
• Successive stages of swallowing are initiated
automatically
• Neuronal areas of reticular substance in
medulla & lower portion of pons initiate
orderly sequence of successive stages
• These areas collectively called deglutition
center
Dr. Misbah-ul-Qamar

28. Constancy of swallowing reflex
• Sequence of swallowing reflex remains same
from one swallow to the next
• Timing of the entire cycle also remains
constant from one swallow to next
Dr. Misbah-ul-Qamar

29. Steps of pharyngeal stage
This stage lasts for less than 1-2 seconds
It is initiated as follows:
1. Soft palate is pulled upward closing posterior nares (Prevents entry
of food into nose )
2. Palatopharyngeal folds approximate medially forming a slit
(Allows masticated food to pass)
Dr. Misbah-ul-Qamar

30. 3rd step
Consists of the following movements
1. Vocal cords are strongly pulled together
2. Larynx is pulled upward and anteriorly by the
neck muscles
3. these actions combined with presence of
ligaments that prevent upward movement of
glottis cause Epiglottis to swing backward over
the opening of larynx
( Prevents entry of food into larynx)
Dr. Misbah-ul-Qamar

31. Actions preventing choking
– Tight approximation of vocal cords (most
essential)
– Movement of epiglottis
• Destruction of vocal cords or of the muscles
that approximate them can cause choking/
strangulation
Dr. Misbah-ul-Qamar

32. 4th step
Following movements take place
1. Upward movement of larynx along with esophagus (Enlarges the
opening of esophagus)
2. Simultaneously Relaxation of upper esophageal sphincter occurs.
This sphincter is called pharyngeooesophageal sphincter also
It is formed by upper 3-4 cm of oesophageal muscular wall
As a result of these movements, food moves easily & freely from
posterior pharynx into upper esophagus
Dr. Misbah-ul-Qamar

33. During 4th step
Sphincter remains strongly contracted between
swallows- prevents air going into esophagus during
respiration
The step provides extra protection against
aspiration
How?
Upward movement of larynx also lifts glottis out of
main stream of food flow
Advantage: food passes on each side of epiglottis,
not over its surface
Dr. Misbah-ul-Qamar

34. 5th step
• Once larynx is raised & pharyngoesophageal
sphincter is relaxed entire muscular wall of
pharynx contracts
– This contraction begins in superior part of pharynx
– Along with contraction, a wave of peristalsis also
begins & spreading in middle and inferior
pharyngeal areas
• Result: food is propelled in esophagus
Dr. Misbah-ul-Qamar

35. Movements of small intestine
Dr. Misbah-ul-Qamar

36. Movements of small intestine
• Like elsewhere in GIT, movements of small intestine are
– Mixing movements: segmentation contraction
– Propulsive movements: peristalsis
• However this categorization is artificial
• All movements of small intestine cause some degree of both
mixing & propulsion
Dr. Misbah-ul-Qamar

37. Segmentation contractions
• How do they arise
• When a portion of small intestine distends with chyme stretching of
intestinal wall Localized concentric contractions at intervals along the
intestine these last for fraction of a minute
• As one set of contractions relaxes, a new set begins
• The new set occurs at new points between previous contractions
Dr. Misbah-ul-Qamar

38. Dr. Misbah-ul-Qamar

39. Segmentation contractions
• These divide the intestine into segments
having appearance of chain of sausages
• Segmentation contractions are slight or absent
between meals but become vigorous after the
meal first enter the intestines
Dr. Misbah-ul-Qamar

40. Control of segmentation movements
• Initiated by: small intestinal pacemaker cells
• Mediated by: enteric nervous system
• Frequency: depend on basic electric rhythm frequency of
electrical slow waves
• In duodenum & proximal jejunum: Normally maximum frequency is not
greater than 12/min
• In terminal ileum: 8-9/min
Factors affecting segmentation
1. Distension of intestine
2. Extrinsic nerve activity
3. Hormones e.g., gastrin
Dr. Misbah-ul-Qamar

41. Role of enteric system in segmentation
• Segmentation contractions become weak
when enteric nervous system is inhibited by
anti-cholinergics (atropine)
• This effect shows that segmentations are not
effective without background excitation from
myenteric nerve plexus
Dr. Misbah-ul-Qamar

42. Function of segmentation
• Is to chop the chyme 2-3 times per minute, mixing it with
secretions of small intestine
• Facilitate the absorption by exposing all parts of
gastrointestinal contents to absorptive surfaces
• Minor propulsion of the chyme as these contractions often
travel 1cm or so in caudad direction
Dr. Misbah-ul-Qamar

43. Propulsive movements of small
intestine
• Chyme is propelled through the small intestine by peristaltic
waves which can occur in any part of small intestine
• the movement of chyme is very slow
• Average rate of movement = 1cm/min
• Are weak, die after travelling 3-5cm.
• Distance covered: These propulsive waves rarely travel farther
than 10cm
Dr. Misbah-ul-Qamar

44. Propulsive movements
• Move toward anus with a velocity of 0.5 -2.0
cm/min
– Faster in proximal intestine
– Slower in terminal intestine
• Time required for passage of chyme from
pylorus to ileocecal valve= 3-5 hours
Dr. Misbah-ul-Qamar

45. Control of propulsive movements in
small intestine
• It can be achieved through
– Nervous signals
– Hormonal signals
Dr. Misbah-ul-Qamar

46. Nervous signals for intestinal
peristalsis
Achieved through
• Distension: by beginning of entry of chyme in
duodenum stretch in duodenal wall
• gastroenteric reflex: initiated by distension of
stomach which spreads down along wall of
small intestine
– It is conducted mainly by myenteric plexus
Dr. Misbah-ul-Qamar

47. Hormonal signals
– Gastrin
– CCK
– Insulin
– Motilin
– Serotonin
All these enhance
intestinal motility
– Secretin
– Glucagon
Inhibit small intestinal
motility
Dr. Misbah-ul-Qamar

48. Function of peristaltic waves in small
intestine
1. Progression of chyme towards ileocecal valve
2. Spreads out chyme along the intestinal
mucosa
– This process intensifies as additional chyme
enters the duodenum
Dr. Misbah-ul-Qamar

49. Peristaltic rush
• It is the powerful & rapid peristalsis taking place in small
intestine
– Normally peristalsis in small intestine is weak
• Peristaltic rush travel long distances within minutes
Cause
• Intense irritation of intestinal mucosa such as in infectious
diarrhea
Dr. Misbah-ul-Qamar

50. Peristaltic rush (cont’d)
• Control of peristaltic rush: Initiated by
• nervous reflexes that involve
– autonomic nervous system
– Brain stem
• intrinsic enhancement of myenteric reflexes within gut wall
• Significance: it sweeps the contents of intestine to colon
• relieves the small intestine of irritation & excessive
distension
Dr. Misbah-ul-Qamar

51. Another motility factor of small
intestine
• Movements are also caused by
– Muscularis mucosae
– Muscle fibers of villi
• These movements are initiated by local
nervous reflexes in submucosal nerve plexus
• Stimulant for this motility: chyme in small
intestine
Dr. Misbah-ul-Qamar

52. Significance of additional motility
• Muscularis mucosae
– can cause short folds to appear in intestinal mucosa
– Mucosal folds increase surface area increased
absorption
• Muscle fibers of villi
individual fibers from muscularis mucosae extend
into villi & cause them to contract intermittently
(shortening, elongating & shortening again)
causes milking of villi lymph flows freely from villi
to lymphatic system
Dr. Misbah-ul-Qamar

53. And then there is MMC
Dr. Misbah-ul-Qamar

54. Paralytic ileus (pseudo-obstruction)
• Trauma to intestines cause a direct inhibition
of smooth muscles which cause decrease
intestinal motility
• Irritation of peritoneum also cause reflex
inhibition due to increased discharge of nor-
adrenergic fibers
• Both types of inhibition cause paralytic ileus
• Due to decreased peristalsis in small intestine,
its contents are not propelled into colon
Dr. Misbah-ul-Qamar

55. Malabsorption by small intestinal
mucosa
sprue
Nontropical and tropical sprue
Dr. Misbah-ul-Qamar

56. Consequences of malabsorption:
1. Steatorrhea
2. Nutritional deficiency
3. Osteomalacia
4. Inadequate blood coagulation
5. Macrocytic anemia
Dr. Misbah-ul-Qamar

57. Large intestine
Dr. Misbah-ul-Qamar

58. Ileocecal juncture
It is a barrier between small and large Intestine
It shows 2 structural features
1. Valve like action of lower end of ileum
2. Ileo-cecal sphincter
Dr. Misbah-ul-Qamar

59. Ileocecal valve
Dr. Misbah-ul-Qamar

60. • Normally about 1500-2000ml of chyme is
emptied into cecum each day
• On reaching the ileocecal valve, chyme is
blocked for several hours, until the person
eats another meal-gastroileal reflex
Dr. Misbah-ul-Qamar

61. • Gastroileal Reflex: After a meal the peristalsis
in ileum pushes the chyme into cecum of large intestine.
Functional significance:
1. Controls progression of chyme from ileum to cecum
Ileileociillecalocecal Valve
Dr. Misbah-ul-Qamar

62. Ileocecal valve
• It protrudes into the lumen of cecum
• It is forcefully closed when excess pressure
builds up in cecum & tries to push cecal
contents backward against valve lips
• It can resist reverse pressure of 50-60cm of
water
Dr. Misbah-ul-Qamar

63. Ileocecal sphincter
• It is formed by thickened circular muscle in the
wall of ileum
• It extends for several centimeters immediately
upstream from ileocecal valve
• It normally remains mildly constricted
• Function: it slows emptying of ileal contents
into cecum
Dr. Misbah-ul-Qamar

64. Control of ileocecal sphincter
Exerted by reflexes from the cecum due to
• Distension of cecum delay in emptying of
chyme
– Contraction of sphincter intensified
– Ileal peristalsis is inhibited
• Irritation of cecum delayed emptying
– In case of inflamed appendix
Dr. Misbah-ul-Qamar

65. Control of ileocecal spincter
• These reflexes are mediated by
– Myenteric plexus in gut wall
– Extrinsic autonomic nerves by way of prevertebral
sympathetic ganglia
Dr. Misbah-ul-Qamar

66. Appendix
• A thin tube about 4 inches long
• It sits at junction of small & large intestine
• Function of appendix is unknown.
• One theory is that the appendix acts as a
storehouse for good bacteria, “rebooting” the
digestive system after diarrheal illness.
Dr. Misbah-ul-Qamar

67. colon
Dr. Misbah-ul-Qamar

68. Principal Functions Of Colon
• Functions of the proximal part of colon
Absorption of water and electrolyte from chyme to form solid
feces
• Functions of distal part of colon
Storage of fecal matter until it can be expelled
 For these functions, no intense movements of colon are
required
Dr. Misbah-ul-Qamar

69. Movements of colon
The movements are sluggish
Characteristics of these movements is similar to
those of small intestine
1. Mixing movements: Haustrations
2. Propulsive movements: Mass Movements
Dr. Misbah-ul-Qamar

70. Mixing movements of colon
• These movements occur in the same manner as segmentation movements
of small intestine
• Sometimes these movements constrict the lumen of colon to occlusion
• Both circular & longitudinal muscle layers take part in these movements
Dr. Misbah-ul-Qamar

71. How haustrations are produced
• Longitudinal layer of smooth muscles in colon is
arranged in form of three bands/strips called
teniae coli
• Large circular constrictions occur in which about
2.5cm of circular muscle contract
• simultaneously tiniae coli also contract
• Circular muscle layer & longitudinal muscles
contract to cause unstimulated portion of colon
to bulge out into bag like sacs- haustrations
Dr. Misbah-ul-Qamar

72. haustrations of colon
• Each haustration reaches peak intensity in
about 30 seconds
• It disappears during next 60 seconds
• New haustral contractions occur in other
areas nearby
Dr. Misbah-ul-Qamar

73. Functions of mixing movements of
colon
• Fecal material is dug into & rolled over 
gradually exposed to mucosal surface of large
intestine
• water and electrolytes are gradually absorbed
until the fecal mass is reduced to 80-200ml/day
• Slow forward propulsion of fecal matter
especially in cecum and ascending colon
Dr. Misbah-ul-Qamar

74. Propulsive movements of colon
• Also called mass movement
• Occur only 1 to 3 times a day
• In many people especially occur after taking first meal of the day
• Once the movement ceases, it returns about half day later
• Usually force a mass of feces into rectum
• A mass movement is a modified type of peristalsis
Dr. Misbah-ul-Qamar

75. How mass movement is produced
 Constrictive ring appears in response to distension/ irritation, usually in
transverse colon
 20 or more cm of colon distal to constrictor ring lose haustrations and
contract as single unit
 This propel the feces (as a single unit) in this segment further down the
colon
 The contraction develops progressively more force for about 30 seconds
 Relaxation occurs during next 2-3 minutes
 Another mass movement then occurs farther along colon
• Series of mass movement persist for 10-30 minutes
Dr. Misbah-ul-Qamar

76. Control of mass movement
• It is initiated after meals
• Facilitated by Gastrocolic and duodenocolic reflexes
• These reflexes result from distension of stomach & duodenum
• the reflexes are mediated by
extrinsic autonomic nerves to colon
Irritation in the colon
Dr. Misbah-ul-Qamar

77. Defecation
• Mass movements force fecal matter into
rectum- desire for defecation occurs
Dr. Misbah-ul-Qamar

78. Rectum
• Most of the time, the rectum is empty of
feces.
How rectum is kept empty?
Dr. Misbah-ul-Qamar

79. How fecal dribble is prevented?
• By tonic constriction of
1. internal anal sphincter: it is several cm long thickening
of circular muscle lying immediately inside anus
2. External anal sphincter: kept continuously constricted
unless conscious signals inhibit it
• composed of striated voluntary muscle
• It surrounds the internal sphincter & extends distal to it
• Controlled by pudendal nerve fibers (part of somatic
system under voluntary, conscious/ subconscious
control
Dr. Misbah-ul-Qamar

80. Weak Intrinsic defecation reflex
Feces enter the rectum
Distention of rectal wall
Afferent signals spread through Myenteric Plexus
Peristaltic wave initiate in descending colon, sigmoid colon
and rectum, forcing feces towards anus
Internal sphincter is inhibited (relaxed)
If external anal sphincter is relaxed by will
Defecation Occurs
Defecation Reflex
Is initiated when a mass movement forces the fecal matter into rectum
Dr. Misbah-ul-Qamar

81. Feces in rectum
Afferent fibres are stimulated & pass to sacral segment of spinal cord
Efferent signals pass through pelvic parasympathetic nerves to descending colon,
sigmoid colon, rectum and anus
Relax internal anal sphincter
Causes weak intrinsic reflex into powerful peristaltic wave
Deep breath, closure of glottis, contraction of abdominal wall muscles
Pelvic floor relax and pull outward on the anal ring to expel the feces
If external anal sphincter is relaxed by will defecation occurs
Parasympathetic defecation reflex
Dr. Misbah-ul-Qamar

82. Pathways of parasympathetic mechanism for enhancing defecation
reflex
Dr. Misbah-ul-Qamar

83. Defecation related effects
Defecation signals entering the spinal cord
initiate other effects;
• Taking a deep breath
• Closure of glottis
• Contraction of abdominal wall muscles
• pelvic floor relax downward and pull outward
on the anal ring to evaginate the feces
Dr. Misbah-ul-Qamar

84. Voluntary activation of defecation
• Defecation reflex can also purposely be
activated
• However reflexes initiated voluntarily are not
as effective as natural reflex
How reflex is initiated?
1. By taking a deep breath downward
movement of diaphragm
2. Forceful contraction of abdominal muscles
increase in intra-abdominal pressure
Dr. Misbah-ul-Qamar

85. Defecation reflex in newborn
• In case of lack of conscious control, defecation
reflexes cause automatic emptying of bowel as
seen in
– Newborns
– In people with spinal cord transection(voluntary
portion is blocked while basic cord reflex is intact)
• Loss of voluntary contraction of external anal
sphincter results in defecation
Dr. Misbah-ul-Qamar

86. Other reflexes affecting bowel activity
1. Peritoneointestinal reflex:
– results from irritation of peritoneum
– Strongly inhibits excitatory enteric nerves
– Can cause intestinal paralysis
2. Renointestinal reflex: kidney irritation
3. Vesicointestinal reflex: bladder irritation
Dr. Misbah-ul-Qamar

87. Functions of colon:
1. Stores and compact the feces
2. Absorption of water
3. Absorption of sodium and chloride
4. Secretion of bicarbonates
5. Bacterial flora synthesize vitamins
like vitamin K, B12 , riboflavin
6. Various gases are produced in colon
by bacterial action on undigested food like carbon dioxide, methane
and hydrogen.
Dr. Misbah-ul-Qamar

88. Dr. Misbah-ul-Qamar

89. Ulcerative colitis
• There is strong hereditary tendency for
susceptibility to ulcerative colitis
• A disease in which extensive areas of large
intestine walls become inflamed & ulcerated
– Motility of ulcerated colon often becomes so great
that mass movements occur much of the day
– Colon’s secretions are greatly enhanced
Dr. Misbah-ul-Qamar

90. Ulcerative colitis (cont’d)
• Cause is unknown
• Treatment options are
– Ileostomy
– Surgical removal of entire colon
Dr. Misbah-ul-Qamar

91. Gastrointestinal obstruction
• Can occur along any point
• Consequences depend on site of obstruction;
• Pyloric , small intestine, large intestine
Dr. Misbah-ul-Qamar

92. Gastrointestinal obstruction:
1. Cancer
2. Fibrotic constriction resulting from
ulcerations
3. Peritoneal adhesions
4. Spasm of a segment of a gut
5. Paralysis of a segment of gut
Dr. Misbah-ul-Qamar

93. Consequences of GI obstruction
Depend on the point in GIT that becomes
obstructed
Obstruction at pylorus (due to fibrotic
constriction after peptic ulceration)
Persistent vomiting of stomach contents
Depression of bodily nutrition
Excessive loss of H+ metabolic alkalosis
Dr. Misbah-ul-Qamar

94. Consequences of GI obstruction
Obstruction beyond stomach
Antiperistaltic reflux starts from small intestine
Intestinal juices flow backward into stomach
These juices are vomited alongwith gastric
secretions loss of water & electrolytes
dehydration with little change in acid base balance
Obstruction near distal end of large intestine
Feces accumulate in colon intense constipation
severe vomiting rupture of intestine+
dehydration+ circulatory shock
Dr. Misbah-ul-Qamar

95. Evacuation of gases from
gastrointestinal tract
• Gases accumulated in GI are classified into 2
groups:
• Exogenous gases– get entry from outside
• Endogenous gases– produced in body
Dr. Misbah-ul-Qamar

96. Exogenous gases
• 90% of accumulated gases
• Enter GI tract by:
– Swallowing through mouth
– Drinking carbonated beverages
Dr. Misbah-ul-Qamar

97. Endogenous gases
• 10% of accumulated gases
• Produced by
– Digestion of food stuff
– Interaction between bacteria & foodstuff in
intestine
Dr. Misbah-ul-Qamar

98. Evacuation of accumulated gases
• By 2 processes:
• Belching
• Flatulence
Dr. Misbah-ul-Qamar

99. Belching (burping)
• A process by which the gas accumulated in
stomach is expelled through mouth.
• Cause: distension of stomach by swallowed air
• Distension causes abdominal discomfort
• Belching expels air & relieves discomfort
• Most of gas is expelled through mouth, only
small amount enters the intestine
Dr. Misbah-ul-Qamar

100. Act of belching
• It requires coordination of several activities:
– Closure of larynx which prevents entry of liquid or
food with air from stomach into lungs
– Elevation of larynx & relaxation of upper esophageal
sphincter. It allows exit of air through esophagus more
easily
– Opening of lower esophageal sphincter
– Descent of diaphragm increased abdominal
pressure+ decrease intra-thoracic pressure
• All these cause expulsion of air.
Dr. Misbah-ul-Qamar

101. Flatulence
• Flatus: production of a mixture of intestinal
gases
• Expulsion of flatus through anus under
pressure is called flatulence
• Quantity: 500-1500ml/ day
Dr. Misbah-ul-Qamar

102. Source of gases in intestine
• Bacterial action on undigested sugars &
polysaccharides
• Digestion of some flatulence producing food
stuff e.g: cheese, yeast in bread, oats, onion,
beans, cabbage, milk
Dr. Misbah-ul-Qamar

103. Dr. Misbah-ul-Qamar

104. Constituents of flatus
• Swallowed nonodorous gases
– Nitrogen
– Oxygen
• Nonodorous gases produced by microbes
– Methane
– CO2
– Hydrogen
• Odorous materials
– Low molecular weight fatty acids like butyric acid
– Reduced sulfur compounds
• Note: ingestion of certain foods such as beans (rich in indigestible
carbohydrates) leads to massive increase in hydrogen content &
increased flatus (symptoms resembling lactose intolerance)
Dr. Misbah-ul-Qamar

105. Dr. Misbah-ul-Qamar

106. Constipation
Slow passage of feces through the large
intestine
Causes slight anorexia, abdominal discomfort
and distention-relieved by evacuation of rectum
Causes:
• Inhibition of normal defecation reflexes
• Vomiting and dehydration
Dr. Misbah-ul-Qamar

107. Causes of constipation
• Confinement to bed
• Hypothyroidism
• Hypercalcemia
• Hypokalemia
• Lead poisoning
• Intake of low fiber
• Spasm of sigmoid colon
• Obstruction of intestinal lumen
Dr. Misbah-ul-Qamar

108. Megacolon (hirschsprung disease)
• Congenitally determined abnormality of
colonic motility
Dr. Misbah-ul-Qamar

109. Diarrhea
• Frequent passage of unformed or liquid stools
• Results from rapid movement of fecal matter
through large intestine
Can be acute or chronic.
Dr. Misbah-ul-Qamar

110. Effects of diarrhoea
• Severe diarrhea with or without vomiting
results in dehydration, hypovolemia,
circulatory shock and electrolyte disturbances
due to loss of gastrointestinal secretions
Dr. Misbah-ul-Qamar

111. Diarrhoea (cont’d)
Types and causes:
• Infections
• Psychogenic diarrhea
• Ulcerative colitis
• Management of diarrhea:
Antibiotics, fluids
Dr. Misbah-ul-Qamar

112. Psychogenic diarrhea
• It accompanies periods of nervous tension
• Caused by excessive stimulation of
parasympathetic nervous system
• This stimulation excites
– Motility of colon
– Excess secretion of mucus in distal colon
• These effects combine to cause marked
diarrhea
Dr. Misbah-ul-Qamar

113. Vomiting
Vomiting is the mean by which upper GIT gets rid of its contents when
any part becomes irritated or over distended
1. Irritation of the mucosa of upper GIT
by irritants or drugs
2. Distension of upper gastrointestinal tract
3. Stimulation of chemoreceptor trigger zone (bilaterally
on floor of 4th ventricle in or above area postrema) by drugs
(opiate, chemotherapy, hormones)
4. Motion, vertigo
Dr. Misbah-ul-Qamar

114. Chemoreceptor trigger zone
• aside from irritative stimuli in GIT, vomiting can also be
caused by nervous signals arising in areas of brain
• One such particular area is called chemoreceptor
trigger zone for vomiting
• it is located in brain medulla  precisely in the area
postrema on lateral walls of 4th ventricle,
• it is responsible for initiation of vomiting by its direct
stimulation through
– Certain drugs( apomorphine, morphine, some digitalis
derivatives)
– Motion sickness
Dr. Misbah-ul-Qamar

115. Dr. Misbah-ul-Qamar

116. Vomiting (cont’d)
Usual stimulus: excessive distension or irritation of duodenum
Afferents: Vagi and sympathetic nerves
Center: near tractus solitarius of medulla
Efferent:
5th , 7th , 9th , 12th nerve to upper GIT
spinal nerves to diaphragm and abdominal muscles
Dr. Misbah-ul-Qamar

117. The prelude to vomiting
• In early stages of irritation or distention,
antiperistalsis begins to occur
• It may begin as far as ileum @2-3cm/sec often
many minutes before vomiting
• It pushes intestinal contents back to stomach
within 3-5 minutes
• Intrinsic contractions occur in duodenum &
stomach along with partial relaxation of
esophageal-stomach sphincter
• Upper portions of GIT become overly distended &
become exciting factor to vomiting
Dr. Misbah-ul-Qamar

118. Mechanism of vomiting:
• Antiperistalsis pushes the contents of upper part
of small intestine to duodenum/stomach_
• over distension of duodenum/stomach
• Taking a deep breath
• Raising the hyoid bone and larynx- upper
esophageal sphincter relaxed
• Closure of glottis
• Lifting of soft palate to close posterior nares
Dr. Misbah-ul-Qamar

119. Mechanism (cont’d)
• Contraction of abdominal muscles and
lowering of diaphragm
• Relaxation of lower esophageal sphincter
• The gastrointestinal contents are ejected
through esophagus
Dr. Misbah-ul-Qamar

120. Dr. Misbah-ul-Qamar

121. Different events which can cause
vomiting
Dr. Misbah-ul-Qamar

122. Motion sickness
• Rapidly changing direction or rhythm of
motion of body can cause vomiting
• Motion stimulation of receptors in
vestibular labyrinth in inner earimpulses are
transmitted to vestibular nuclei of brain
stem to cerebellum to chemoreceptor
trigger zone vomiting
Dr. Misbah-ul-Qamar

123. Nausea
• Is conscious recognition of subconscious
excitation in an area of medulla in close
association with or part of vomiting center
• Sensation is often a prodrome of vomiting
• Only certain portions of vomiting center are
associated with nausea
– (as indicated by occasional vomiting without
nausea)
Dr. Misbah-ul-Qamar

124. Causes of nausea
Can be caused by;
1. Irritative impulses coming from
gastrointestinal tract
2. Impulses that originate in brain stem
associated with motion sickness
3. Impulses from cerebral cortex to initiate
vomiting
Dr. Misbah-ul-Qamar

125. Dysentry
Acute inflammation of large intestine
characterized by frequent loose stools mixed
with blood and mucus
Dr. Misbah-ul-Qamar