Choudhury GI Physiology Flashcards
Salivary glands
and secretion
submandibular: serous/mucous
sublingual: serous/mucous
parotid (largest): serous
smaller glands: mucous
(buccal, lips, tongue, palate)
Functions of Saliva:
Taste Lubrication Protection Digestion Speech Not essential for life
Saliva – composition & function
water, mucus- facilitates speech, dissolving, tasting food, swallowing; food into cohesive bolus
alpha amylase- carbohydrate digestion, cleaves a-1,4 glycosidic bonds in starch,
lingual lipase, ribonucelase- initiates fat digestion, hydrolysis of dietary lipid RNA digestion
lysozyme- antibacterial (bacillus and streptococcus), innate and acquired immunity
lactoferrin- chelates iron (inhibits microbial growth)
lactoperoxidase- antibacterial (kills bacteria in milk and mucosal lining)
glycoprotein of IgA- secretory IgA- immunologically active against virus and bacteria
EGF, NGF- mucosa growth adn protection
kallikrein- activates bradykinin- dilates arterioles, constricts veins, increases blood flow to secretory glands
bicarb- minimizes tooth decay (neutralizes bacterial acid), neutralizes refluxed gastric acid into lower esophagus (heartburgn)
hypotonis, low osmolality– taste (carbs and fats, not protein)
Two types of salivary glands:
- serous (parotid- secretes nonviscous saliva composed of water, electrolytes and enzymes)
- mixed (submandibular, sublingual- secretes viscous saliva rich in mucin glycoproteins)
salivary Acini:
primary secretion-saliva, plasma (H2O, Na+, Cl-, K+, HCO3-, amylase)
salivary Myoepithelial cells:
motile, contracts, expels saliva
salivary glands- ductal
modifies secretion by modifying electrolytes, Na+, Cl- reabsorbed K+, HCO3- secreted
Striated duct epithelium tight junction - H2O cannot leave duct
**Ductal cells are water impermeable, water is not
absorbed along with the solute, water remains
in lumen and saliva is secreted hypotonic relative
to plasma
Salivary secretion – acinar & ductal cells
Initial saliva is produced by acinar cells
Subsequently modified by ductal
epithelial cells
Salivary ducts are impermeable to water
and sodium is continually reabsorbed
Lumen of ductal cells contains
3 transporters:
- Na +- H + exchange,
- Cl - HCO 3 exchange, and
- H +- K + exchange
Basolateral membrane contains:
- Na +/K + ATPase and Cl channels
Net absorption of Na + & Cl causes
NaCl in saliva lower than in plasma
Net secretion of K + and HCO 3 causes
K + and HCO 3 in saliva higher than in
plasma
Salivary secretion – rate & composition
**Ionic composition of saliva changes as salivary flow rate changes
Duct cells modifies the composition of saliva
At highest flow rates (4 mL/min), final saliva resembles plasma (high Na+, Cl-, low K+)
as the ductal cells have less time to modify the saliva
At lowest flow rates (< 1 mL/min), final saliva is dissimilar to plasma (low Na+, Cl-, high K+)
as saliva has more contact time with ductal cells, more Na+ and Cl- are reabsorbed, which
decreases their concentration and more K+ is secreted (hypotonic)
Salivary secretion - regulation
Salivary secretion and composition are controlled mainly by the ANS and to a lesser extent by hormones
Parasymp plays a major role
Parasymp stimulates & inhibits profoundly than Symp
Stimulated: by smell, taste, sound, sight, chewing, spicy or sour tasting foods, smoking.
Inhibited: by sleep, fear, anti-cholinergic & anti-depressant medication, dehydration, fatigue.
Modulated: by blood secretion, myoepithelial cell contraction, hormonal secretion.
Xerostomia
dry mouth due to absence of saliva production (drugs, radiation treatment, autoimmune disease).
buccal infections/dental caries
very common symptoms
Sjogren’s syndrome
autoimmune process-targets salivary and lacrimal glands
glandular atrophy and decreased saliva production (xerostomia), dry eyes (keratoconjuctivitis sicca)
difficulty in chewing, swallowing and speech.
dry oral mucosa, superficial ulceration, buccal infections/dental caries
Drooling
excessive salivation due to increase nervous stimulation
treatment: anticholinergics and surgical removal of sublingual glands
Parkinson’s, tumors of mouth/esophagus
increased saliva production due to unusual local reflexes and increase neurological stimulation
Cystic fibrosis
elevated Na+, Ca2+ and protein in saliva, sweat, pancreatic fluid & bronchial secretion
CF patients lacks CFTR or chloride transporter
Addison’s
increase Na+ in saliva (↓ Na+ reabsorbed)
Primary aldosteronism & Cushing’s
decrease Na+ in saliva (↑ Na+ reabsorbed), salivary NaCl is zero, increase K+ levels
Digoxin therapy
increase Ca2+ & K+ in saliva
Esophagus
motility
Esophageal motility is under both voluntary and involuntary control, peristalsis
Esophagus muscle composition:
- upper third (UES)– skeletal muscle, under voluntary control
- middle third – mixture of skeletal and smooth muscle
- lower third (LES) – smooth muscle, regulated by autonomic nervous system and enteric nerve plexus
Swallowing and opening of UES
- relaxation of UES and allows food to enter esophagus from pharynx, sphincter then closes
- coordinated by the brain stem, initiates local reflex and swallowing causes primary peristalsis
- distention of esophagus causes secondary peristalsis
Opening of LES
- when not eating LES remains closed (tonically constricted) due to sphincter pressure by diaphragm
- when eating, LES relaxes in response to swallowing and distention of esophagus
- this relaxation is mediated both by vagal stimulation and intrinsic properties of LES
Common disorders of esophageal function
GERD: gastroesophageal reflux disease, common
Barrett’s esophagus: special type of GERD
Dysphagia: difficulty in swallowing
Achalasia: failure of LES to relax, food in LES
Incompetent LES: failure of LES to contract
Diffuse Esophageal Spasms: uncoordinated
esophageal contraction
Hiatal Hernia: moves LES into thoracic cavity, increased
gastro-esophageal reflux
Barrett’s esophagus
(pre-cancerous lesion):
it is most often diagnosed in people who have long-term GERD (chronic inflammation)
this condition is recognized as a complication of GERD
a condition in whichcolumnar cells replace squamous cell in themucosa of esophagus
the main cause of Barrett’s esophagus is thought to be an adaptation to chronic acid
exposure fromreflux esophagitis
its importance lies in its predisposition to evolve into esophagealcancer
it develops in about 10–20% of patients withchronic GERD.
Achalasia
** bird’s beak
Achalasia (failure to relax):
special form of dysphagia
complete lack of peristalsis within esophagus
LES does not relax and increased LES pressure
food is retained at the level of LES
caused by:
- nerve degeneration (enteric nervous system)
- lack of NO synthase, VIP, etc
- Chagas disease (infection protozoa: Trypanosoma cruzi)
Diffuse Esophageal Spasms
diffuse esophageal spasms (DES) are irregular, uncoordinated, and sometimes powerful
–> CORKSCREW appearance
in some, very hot or very cold foods may trigger an episode
Hiatal Hernia
a hiatus hernia or hiatal hernia is the protrusion (or herniation) of the upper part of the stomach into the thorax through a tear or weakness in the diaphragm
in hiatal hernia, it is easier for stomach acids to come up into the esophagus
this causes a burning feeling in the throat and chest
symptoms similar to GERD
