1. Salivary secretion, swallowing and esophageal motility and vomiting Dr
Salivary secretion, swallowing and esophageal motility and vomiting Dr. Mukhallad Al Janabi MD, MSc, PhD
OBJECTIVES:
1. Describe the physiological role of various salivary glands.
2. Describe the components and functions of saliva.
3. Describe the neural regulation of salivary secretion.
4. Predict the components of salivary secretion at different flow rates.
5. Describe the neural and muscular events that mediate swallowing.
6. Describe the mechanism of swallowing phases (oral, Pharyngeal, and esophageal).
7. Discuss the neural control and the mechanism of vomiting.

2. **Chewing and Swallowing
Today lecture
**Salivary secretion
Composition and functions of saliva
Control of salivary secretion
**Chewing and Swallowing
Stages of swallowing
**vomiting

3. Saliva Salivary Flow: *1-1.5 L/day
Introduction
The Major Salivary Glands:
*Parotid-produces serous secretion containing alpha amylase enzyme (ptyalin)
*Submandibular-produces serous and mucous secretion
*Sublingual-similar to submandibular secretion
*The Minor Salivary Glands- buccal glands secret only mucus
Salivary Flow:
*1-1.5 L/day
**Major flow in unstimulated state comes from Submandibular
**Major flow in stimulated state comes from Parotid
Salivary α-amylase (ptyalin) is produced predominantly by the parotid glands, and mucin is produced mainly by the sublingual and submandibular salivary glands

4. Innervation of salivary glands
Saliva production is controlled by salivary center in medulla through autonomic nervous system. Salivary secretion is the only digestive secretion that controlled only by neural factors
*Excitation of parasympathetic nerve fibers causes:
Copious (present in large quantity) watery secretion rich in electrolytes and enzymes
*Excitation of sympathetic nerve fibers causes:
-slight increase in viscid saliva (containing mucus)
Salivary secretion is increased by
1. Tactile stimuli in mouth
Acid in the mouth
Stimulating oral touch receptor
2. Thinking & smelling of appetizing food
Salivation is increased when there is imminent vomiting

5. Basic saliva components
• Water
• Ions: Na+, K+, Ca2+, Cl–, HCO3–
• Proline-rich proteins for protection of teeth enamel:
Enzymes: ptyalin (from salivary glands),
**lingual lipase (secreted from glands on the tongue).
Immunoglobolins: IgA
Mucin: glycoproteins for lubrication of food and protection of oral mucosa
ABO blood group antigens
• Lysozyme, lactoferrin, thiocyanate ions
pH of saliva is about 7

6. Function of Saliva
 1. Moistens oral mucosa. The mucin layer on the oral mucosa is thought to be 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. Buffers oral cavity contents. Saliva has a high concentration of bicarbonate ions. It help in maintaining the oral pH around 7. It neutralizes any gastric acid that refluxes from stomach 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. Saliva is high in calcium and phosphate. It helps to minimize tooth decay

7. Function of Saliva (cont
Function of Saliva (cont.) Saliva plays an important role in the general hygiene of the oral cavity
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.
***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.
b. The flow of saliva helps to wash away pathogenic bacteria and food particles that provide metabolic support for bacterial growth.
Some of intraoral complications of salivary hypofunction include
Candidiasis 
Recurrent aphthous ulcers (blister on the
mucous membranes)  
3. Dental caries.

8. General structure of the salivary unit

9. Transport processes causing the formation of saliva
***Saliva contains more K+ , HCO3– and less Na+ , Cl– compared to plasma.
** saliva produced by acinar cells has almost the same composition of the plasma. In 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.

10. 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 mmo/l,
K + : 30
HCO3-: 50
***When salivary glands are stimulated maximally and the flow is increased, the conc. of ions is less changed and conc. of Na + and Cl- is half or two third of plasma conc. and K + conc. is four times of the plasma conc.
*** the salivary ducts are relatively impermeable to water
*** saliva is hypo-osmotic solution
There is excess sodium reabsorption over potassium secretion

11. Mastication (chewing)
Chewing: is the first stage of food ingestion
** It is important for digestion of food because
1. It breaks the cellulose membrane of the fruits and vegetables.
2. It increases the surface area on which digestive enzymes work
3. It prevents excoration of gatrointestinal tract.
Chewing reflex:
Presence of food bolus causes dropping of the lower jaw. This stretch the mastication muscles which causes reflex contraction of mastication muscles (Stretch reflex). Contraction of mastication muscle will elevate lower jaw so the bolus stimulates mouth lining and this initiates another reflex. This reflex repeats itself again and again until the bolus is swallowed.

12. Swallowing (deglutition)
Is the second stage of food ingestion
It consists of three stages
Voluntary stage- initiation stage
Pharyngeal stage
Esophageal stage
Involuntary stages

13. Tongue presses the hard palate
(1) Voluntary phase
Bolus of food
Swallowing is initiated by closing the mouth and pushing voluntarily the bolus by the tongue posteriorly and upward against the palate
Tongue presses the hard palate
forces the bolus to oropharynx
Tonsillar pillar areas 13

14. (2) Pharyngeal phase
Reflexly Nasopharynx closed by elevation soft palate
**The second stage starts when the bolus reaches posterior part of the mouth and early parts of pharynx.
**It is involuntary action and reflex in nature.
**Presence of food in above places stimulates pressure receptors there specially on tonsillar pillars. Sensory impulses carried to swallowing center in brain stem through trigeminal and glossopharyngeal nerves.
Epiglottis closes the larynx
Bolus entering esophagus and UES relax 14

15. Pharyngeal stage (cont.)
Impulses coming from swallowing center to pharynx and esophagus to finish stage 2 and 3 of the swallowing act. In pharyngeal stage, the following events occur:
1. pushing the soft palate upward to prevent reflux of food to nasal cavity.
2. to prevent passage of food into trachea. This done by:
The vocal cords are approximated
The larynx is pulled upward
Epiglottis swing back over the opening of larynx.
3. Palatopharyngeal folds are pulled medially forming slit through which the good masticated food can pass easily.
4. Relaxation of upper esophageal sphincter
5. Pharyngeal muscle contraction starts (peristalsis) from upper parts and spreading down ward

16. Pharyngeal stage (cont.)
At the beginning of stage two, inhibitory impulses from swallowing center to respiratory center to stop respiration at any point of respiratory cycle.
Pharyngeal stage lasts for less than two seconds
The upper esophageal sphincter (the upper 3 cm of esophagus) is closed all the time except during swallowing.
**the 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.

17. (3) Esophageal stage
Movement of bolus through esophagus is through peristalsists:
Primary peristalsis is continuation of pharyngeal peristalsis which takes 8-10 second to travel along the esophagus. This peristalsis is capable to push the bolus down ward. Bilateral cervical vagotomy will abolish this peristalsis.
Secondary peristalsis starts if primary peristalsis fails to push the bolus downward and will continue until the esophagus is empty. This peristalsis is initiated by distention of the esophagus by retained food. It is due to stimulation of the myentric plexus in the wall of esophagus and it will continue after vagotomy

18. Esophageal stage (cont.)
Lower esophageal sphincter (LES)
**Is located 3 cm above the junction between esophagus and stomach . It remains contracted all the time except during esophageal stage of swallowing. The LES is relaxed by receptive relaxation mechanism ( during peristaltic contraction the part in front of contraction part is relaxed by inhibitatory neurons in myentric plexus.
*** 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.
When intra-abdominal pressure is increased during coughing, the lower portion of the esophagus is closed by valve like action of this part

19. Receptive relaxation of the Stomach
Bolus of food
LOS opens
Due to wave of relaxation transmitted through Myenteric
Inhibitory
Neurons
Relaxed muscles
Relaxed
muscles
Stomach
Stomach 19

20. VOMITING (EMESIS) ACT The sudden and forceful expulsion of gastric
and upper intestinal contents
* It is controlled by neurons in medulla (the ‘vomiting centre’)
*It is triggered by one or more of the following stimuli:
- excessive gastric or duodenal distension
- noxious substances in stomach
- certain smells or sights
- emotional factors
- touch receptors at back of throat
- reflexes involving semi-circular canals (‘motion
sickness’)
- stimulation of the ‘chemoreceptor trigger zone’ by circulating ‘emetics’

21. 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 fourth ventricle of the brain.
** is 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.

22. THE VOMITING REFLEX SEQUENCE OF EVENTS
It starts by salivation and sensation of nausea
• 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
***Vomiting act is accompanied by generalized autonomic effects e.g:
- sweating
- tachycardia
- 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