1st lecture

Gastrointestinal system
⩥This is our 1 lecture for this system, hope you enjoy the content.
st

∵ first of all, when a person eats, ingested food goes through 2

Processes at first, which are chewing (mastication) then
Swallowing (deglutition) in this lecture we’re discussing that.

↬Chewing: 1 st
stage of ingestion and is the act of cutting(incisors),
grinding(molars), mixing, Lubricating, partially digesting food to
swallow, it’s significance that it:
1. breaks indigestible Cellulose of fruits & vegetables
2. it increases the surface area when crushing the food
(As digestive enzymes exert their effect on the surface of molecules only)
3. it prevents excoriation of gastrointestinal tract.

⨠The mechanism of chewing:

⇾Presence of food in the mouth causes dropping of lower jaw (stretch inhibition) this drop
causes stretching of mastication muscles which will initiate stretch reflex, causing rebound
contraction (response to passive stretching of muscles) which raises the lower jaw and causes
closure of teeth, when the lower jaw is raised it compresses the bolus against the lining of
mouth stimulating it which initiates reflex inhibition and dropping of lower jaw again and so on
until the bolus is swallowed.

↬Swallowing: 2 stage of ingestion moving the food from pharynx to stomach and is
nd

composed of 3 stages.
⨠ The mechanism of swallowing:
A. voluntary stage: initiated by closing the mouth and pushing the bolus voluntarily by the
tongue backward and upward after this, swallowing becomes automatic and ordinarily
cannot be stopped.

B. Pharyngeal Stage of Swallowing: initiated when the bolus enters the posterior mouth
and pharynx, it stimulates swallowing(pressure) receptors especially on the tonsillar
pillars(greatest sensitivity), and impulses from these pass to the brain stem’s (through
glossopharyngeal and trigeminal nerves) swallowing center, which causes the following
sequence of events to happen:
 Gastrointestinal system

1.The soft palate is pulled upward to close the posterior nares, to prevent reflux of food
into the nasal cavities.

2. The palatopharyngeal folds are pulled medially Forming a sagittal slit that allows
“selectively” the passage of properly chewed food, others are delayed till chewed.

3. vocal cords get strongly approximated, larynx is pulled upward and anteriorly by the
neck muscles, then ligaments that prevent upward movement of the epiglottis causes it
to swing backward over the opening of the larynx.
⇢Approximation of vocal cords is the most important, as the epiglottis
doesn’t close the inlet to the larynx completely (it mainly directs the food bolus).
4. Then esophagus is wide opened as a result of:
a. larynx upward movement enlarges it’s opening and away from the
main stream of food
b. upper esophageal (pharyngoesophageal) sphincter relaxation.
5. finally pharynx contracts, beginning with superior part till the inferior, propelling food
to esophagus to continue it’s peristaltic movement.

⇝Quick summary: trachea is closed, the

Esophagus is opened, and a fast
peristaltic wave initiated by the nervous
system of the pharynx forces the bolus
of food into the upper esophagus,
the entire process occurring
in less than 2 seconds.

⇒At the beginning of stage two, inhibitory impulses from swallowing center to
respiratory center to stop respiration at any point of respiratory cycle.

⇒The upper esophageal sphincter (the upper 3 cm of esophagus) is closed all the time
except during swallowing.

⇒Sensory information initiating swallowing reflex is carried by 5th and 9th cranial
nerves. The motor orders from swallowing center to pharynx and esophagus are through
5th,9th,10th,12th cranial verves and few upper cervical spinal nerves.
 Gastrointestinal system

C) Esophageal stage: esophagus main function is to conduct food to stomach, doing

that through 2 types of peristaltic movements.

Ⅰ. Primary peristalsis: continuation of pharyngeal peristalsis, takes 8-10 second to

travel along the esophagus, pushing the bolus downward. When standing upright, it will
take less time(gravity)
-Bilateral cervical vagotomy will abolish this peristalsis approximately 5-8 seconds

Ⅱ. Secondary peristalsis: happens when esophagus gets distended as a result of

retained food after failure of primary peristalsis.
secondary peristaltic waves continue until all the food is emptied into the stomach.
It is due to stimulation of the myenteric plexus in the wall of esophagus (it
will continue after vagotomy) then transmitted upward through vagal afferent fibers
to the medulla and back again to the esophagus through glossopharyngeal and
vagal efferent nerve fibers.

Because last 8th of esophagus is

more resistant to gastric acids so
LES remains contracted

⨠lower esophageal sphincter (Gastroesophageal Sphincter): 3 centimeters above

esophageal juncture with the stomach, circular muscles thickens and function as lower
esophageal sphincter.

⇾Remains contracted?(with intralumenal pressure of 30 mmHg), except during

esophageal stage it relaxes, on the other hand the midportion remains relaxed
normally.
⇾ LES is important to prevent reflux of
stomach content into esophagus.
⇾pressure in LES is about 30 mm Hg
⇾failure of LES relaxation causes achalasia
⇾failure of LES contraction causes reflux of
stomach content to esophagus causing reflux
esophagitis (Gastroesophageal reflux disease) GERD
 Gastrointestinal system

∵Receptive relaxation of stomach: when the peristaltic wave approaches the

stomach it is transmitted through inhibitory neurons of myenteric plexus causing
entire stomach to relax and duodenum to a lesser extent, giving the stomach ahead of
time to receive propelled food.

∵Vomiting: The sudden and forceful expulsion of gastric and upper intestinal
content OR, it is how GIT reacts to irritation of mucosa, over distention of tract or
overexcitation, of any part of it, but duodenum provides stronger stimulus.

►Triggers:
1)excessive gastric or duodenal distension and irritation
2)noxious substances in stomach
3)certain smells or sights
4)emotional factors
5)touch receptors at back of throat
6)reflexes involving semi-circular canals (‘motion sickness’)
7)stimulation of the ‘chemoreceptor trigger zone’ by circulating
‘emetics’ or electrical impulses

∵How do we vomit:
►at first Stimulus (from stomach, esophagus or duodenum) transmitted
through Sympathetic and vagal afferent fibers to the vomiting center in BS.

►from there motor signals are transmitted as follows:

1)Upper GIT by the 5th ,7th ,9th ,10th, and 12th CN.
2)lower tract through vagal and sympathetic nerves.
3)diaphragm and abdominal muscles through spinal nerves.
►resulting from motor signals this sequence of events:
• Deep inspiration, respiration held in mid inspiration
• Closure of glottis
• Relaxation of lower esophageal sphincter
• Contraction of diaphragm and abdominal muscles causes
increased intra-abdominal pressure
• Duodenal contraction (reverse peristalsis).
• Rapid rise in intra-gastric pressure causes reverse expulsion of
gastric and upper parts of small intestine contents
 Gastrointestinal system
∵VOMITING CENTER:
is found in reticular formation of medulla and pons
receives sensory impulses from pharynx, esophagus, stomach and upper parts of
small intestine.
sensory impulses reaching it from GIT are carried by both afferent sympathetic
and parasympathetic fibers.

∵chemoreceptor trigger zone:

►is located on the lateral wall of lower end of the fourth ventricle of the brain.
►stimulated by certain drugs like morphine, apomorphine, digitalis, circulating
emetic substances for example substances accumulated in the blood of renal
failure patients.
►it is also stimulated by impulses coming from vestibular apparatus.
Destruction of this area
-Area postrema (CTZ part of blocks chemical induced type
It) isn’t covered by BBB, of vomiting but does not
block vomiting resulting from
circulating emetics and irritative stimuli in the
chemotherapy can cause gastrointestinal tract itself.
vomiting.

►it is worthy to note that vomiting resulting from motion sickness happens as
follows:
Stimulation of vestibular labyrinth ⇶vestibulocochlear N⇶ vestibular nuclei
⇶CTZ⇶ vomiting center ⇶ vomiting.

►vomiting comes with autonomic effects like sweating, tachycardia, and

salivation.
►Vomiting of gastric content alone for prolonged time (for example in pyloric
stenosis) leads to metabolic alkalosis While vomiting of large amount from
duodenum causes metabolic acidosis.
 Gastrointestinal system

∵salivary secretions
Minor glands like buccal glands secrete mucin

►saliva comes mainly from major salivary glands

Which are: -Ptyalin digests starch
1)parotid gland: produces serous secretion -mucus is important for lubrication,
Bringing food together and
containing alpha amylase enzyme (ptyalin) protection of surfaces.
-when eating(stimulated) majority of
salivary content comes from it.

2)submandibular: produces serous and mucous secretion.

- when mouth empty (non-stimulated) majority of
salivary content comes from it.
3)sublingual: serous and mucous secretion like submandibular.
-Salivary flow is 1-1.5 L daily
► Salivary α-amylase (ptyalin) is produced
predominantly by the parotid glands, and
mucin is produced mainly by the sublingual
and submandibular salivary glands.
∵Innervation of salivary glands:

►saliva is controlled only by neural factors, by salivary center in medulla through

ans.
►Two cases of saliva production:
1)PS stimulation:
-Increases secretion greatly
-secretion is watery(copious)
-rich in electrolytes and enzymes
2) Sympathetic stimulation:
-secretion increases slightly
-secretion is viscid(mucoid)
-constriction of blood vessels
supplying glands.

►salivary secretion is increased by:

1. Tactile stimuli in mouth: a) Acid in the mouth
b) Stimulating oral touch receptor
2. Thinking, tasting & smelling of appetizing food.

►salivation also increases as a protective mechanism when there is imminent

vomiting.
 Gastrointestinal system

∵structure of the salivary unit:

acinus ⇢intercalated duct ⇢intralobular duct

⇢interlobular duct ⇢main pancreatic duct.

∵Formation of saliva:

►saliva produced has the same composition as plasma, then it

is modified along it’s way in the ducts.
►the salivary ducts saliva composition is altered by absorption
of Na+ and Cl– from the saliva and secretion of K+ and HCO3-
into saliva.
►Na+ absorption and K+ secretion is increased by aldosterone.
i.e aldosterone increases K+ and reduces Na+ conc. in saliva.
►Electrolyte composition of the saliva is modified by
selectively reabsorbing sodium and selectively secreting
potassium and bicarbonate.

►salivary components are:

1)Water (90-96) % 2) Ions: Na+, K+, Ca2+, Cl–, HCO3 –
3)Proline-rich proteins for protection of teeth enamel
4)Enzymes: ptyalin (from salivary glands), lingual lipase (secreted from Von
Ebner gland on posterior the tongue).
5)Immunoglobulins: IgA
6)Mucin: glycoproteins for lubrication of food and protection of oral mucosa
7)ABO blood group antigens
8)Lysozyme, lactoferrin, thiocyanate ions

-pH of saliva is 6-7

-The more the flow of saliva, the
least the modification, the closer it
will be to plasma composition.
-The least the flow of saliva the
more the modification the further
it will be from plasma
composition.
 Gastrointestinal system

∵Function of saliva:
1)Moistens oral mucosa, mucin layer is the most important
nonimmune defense mechanism in the oral cavity, it facilitates speaking
chewing and swallowing.
2)Help to moisten, lubricate and soften food, mixes it up and makes it possible
to be swallowed.
3)Provides a medium for dissolved foods to stimulate the taste buds.
4)it has high bicarbonate so it Buffers oral cavity contents, maintains the oral
pH at 7 neutralizes gastric acid into the lower esophagus.
5)Digestion: Alpha-amylase, contained in saliva, breaks starch and glycogen,
while lingual lipase helps break down fats.
6)Mineralization of new teeth and repair of precarious enamel lesions, it is
high in calcium and phosphate. It helps to minimize tooth decay.
7)Protects the teeth by saliva protein which contains antibacterial compounds.
Thus, problems with the salivary glands generally result in dental caries.
8)Controls bacterial flora of the oral cavity through a. Presence of Lysozyme,
Secretory IgA, and Thiocyanate ions. All play important roles in saliva’s
antibacterial actions.
9)Lysozyme attacks bacterial wall.
-IgA interferes with the adherence of microorganisms to host tissue. It
neutralizes viruses, bacterial, and enzyme toxins.
-also, saliva contains lactoferrin which binds free iron in the saliva causing
bactericidal or bacteriostatic effects on various microorganisms requiring iron
for their survival.
-flow of saliva helps to wash
away pathogenic bacteria and
food particles that provide
metabolic support for bacterial
growth.
►salivary absence(xerostomia) causes:
1. Candidiasis
2. Recurrent aphthous ulcers (blister on the mucous membranes)
3. Dental caries.
 Gastrointestinal system

∵Regulation of salivary secretion by PSNS

►additional vasodilation can be caused by kallikrein(enzyme) secreted by the

activated salivary cells, which splits alpha2globulin of blood, to form bradykinin,
a strong vasodilator.

⋗ Variation in osmolality and ion composition of saliva with flow rates:

► At resting condition flow of saliva is slow so the modification in
composition will be more.
In this state the conc. of ions as follows:
- Na+ and Cl-: 15 mmol/L
- K +: 30
- HCO3-: 50 (independent on flow rate)
►When salivary glands Stimulated maximally
⇶ flow is increased ⇶ the conc. of ions is less
Changed ⇶ conc. of Na+ and Cl- is 1/2 or 2/3rd
Of plasma conc ⇶ K + conc. is 4x of the plasma
conc.
*The salivary ducts are relatively impermeable
to water.
*Saliva is hypo-osmotic solution.
- There is an excess sodium reabsorption
over potassium secretion.