GI: Motility and Secretion; Oral Cavity, Stomach-Mahmoud

What is mastication, what is involved

Chewing, where the tongue and teeth are involved

What is the purpose of chewing? Name 5 fxns.

Size reduction, Mixing, Propulsion, Taste, and protectin by release of immunological salivary agents

is chewing and essential part of digestion? what happens when you cant chew?

No, as long as food stuff is small enough to pass into the pharynx
Seen with edentulous (toothless) pts. Food is larger and dry. Lead to less savor time and weight loss.

What is the composition of Saliva?

Mucin, Elctrolytes, Enzymes, Bacteriocidal, Blood groups, and IgA

What are the functions of saliva

1)Lubrication: Swallowing, speech
2)protection:Dilutes buffers, cools/warms
3)hygiene: rinsing, immune and bacteriocidal component
4)digestion: Carbohydrates and Lipids

How much saliva is secreted per day by salivary glands

1-1.5L/day

What is special about blood flow rate in the salivary glands

High blood flow rate; for fluid and electrolyte eflux into the mouth

What is the basic cell unit for salivary gland

Salvion

What is the pathway of saliva in the salivary gland

Starts in the Acinus (round sac end), pushed through the intercalated duct(isotonic/neutral) by myoepithelial cells then into the striated duct (reabsorbs NaCl) at the end of the gland into the oral cavity (hypotonic/alkaline)

What is the saliva modified as it moves through the salvion gland

it is isotonic and neutral at first and becomes more hypotonic and alkaline

What cell types is the acini composed of, and what do they produce

Serous: bigger cells, watery saliva with alpha amylase
Mucous: smaller cells, thicker saliva rich with mucins (lubricate food for swallowing

How is salivation rate controlled, which control is more dominant

Through Parasympathetic and Sympathetic ANS, both work to INCREASE salivation rate
P-ANS is more DOMINANT through blood flow and acini activity
S-ANS works through myoepithelial control

What are some physiological stimulators of salivation

Chewing, Tasting, smelling food, and nausea

What are some physiological inhibitors of salivation

Sleep, fatigue, dehydration, and fear

What are the two functions of the esophagus

To act as a barrier, and to aid in propulsion of food

What are the two barriers of the esophagus

Upper and lower esophagus sphincters

What is the route of the esophagus to the stomach

It passes between the pleural space b/w the lungs and thoracic wall

How does negative PpI effect air and gastric acid in relation to the esophagus, what is need to prevent this?

Entry of Air and stomach Gastric secretions are favored into the esophagus; the upper and lower sphincters are needed to prevent their entry

What is a hiatus hernia

incompetence of the LES; can be the cause of severe reflux disease

What are some effects of gastric reflux

Barrets esophagus, with low to high grade dysplasia
cells will proliferate

What is swallowing and what does it control/prevent

Coordination of the mouth, pharynx and esophagus to allow the passage of food bolus into the esophagus and prevent aspiration in to the nasal cavity and trachea

What are the two stages of swallowing

Voluntary and involuntary

What is the voluntary stage of swallowing

starts when food moves into the oropharynx by movements of the tongue

What are the three steps of the involuntary stage in swallowing

1) the nasopharynx closes by contraction of the pharyngeal muscles
2) trachea closes
3) relaxation of the UES and propulsion of food into the esophagus

What is inhibited during swallowing

Ventilation and speech

What are the steps of the swallowing reflex

Food bolus--> pharyngeal receptors--> Afferent (Vagus. Glossopharyngeal) --> medullary center--> actions (closing of nasopharynx, trachea and propulsion into esophagus

Dysphagia

Difficulty swallowing due to mechanical or neural factors.

What is primary peristalsis

Initiated through pharyngeal receptor contact to propel food down the esophagus to the stomach; initiated by swallowing

What is secondary peristalsis

Similar to primary but initiated by distention of the esophagus by material in the lumen

What is the fxn of the secondary peristalsis

To clear or "sweep" the esophagus of Residual Food Particles or to remove gastric reflux

How is esophageal motility controlled

ANS control of the UES/ LES and smooth muscles of peristalsis

What controls most actions of motility in the esophagus

Vagus nerve, the meduallary swallowing center, and the myenteric plexus

How is tonic closure of the UES controlled

intrinsic pharyngeal muscle tone between swallows

What controls relaxation of the pharyngeal muscle

Vagus nerve and the medullary swallowing center

How is esophageal body peristalsis controlled (2)

Vegus nerve innervation of the smooth muscle layers
Enteric neurons (myenteric plexus) integrate info and also control peristalsis intrinsically

How is tonic closure of the LES controled

Intrinsic myogenic control, constricting in response to passive stretch

How is relaxation during swallowing controlled

Inhibitory reflex integrated by the Vagus nerve

Achalasia

High LES tone and failure to relax during swallowing.
degeneration of the ganglion cells of the myenteric plexus impair LES relaxation

What are some motility regions of the stomach

Orad, Caudad, Pyloric Sphincter

Orad region of the stomach

fundus and proximal part for volume accomodation and gastric emptying

Caudad Region of the stomach

Antrum and Distal part for mixing and propulsion

Pyloric Sphincter

Gastric empyting

Muscle histology of the stomach; what is a new muscle found only in the stomach

Longitudinal and circular smooth muscle like the rest of the GI tract. Also has oblique muscle for mixing and propulsion

How does the layering of the smooth muscle change along the stomach

increases as you move towards the caudad region due to specific motility actions

What controls motility activities that effect gastric emptying rates

Neural and hormonal controls

In the stomach what speed ups and slows down gastric emptying

Gastric filling

What part of the GI has a greater and potent effect on gastric empyting

The duodenum, by feedback sensing of the chemical and nutrient make up of the chyme, through neural and hormonal control

How does chyme composition (when comparing macronutrients) effect gastric emptying

rates of emptying are Carbohydrate>Protein>Lipids
Regulated by cholecyctokinein

What GI hormone regulates slowing of gastric emptying in response to high lipid content

cholecystokinein CCK

Why is there a delayed response to fat in gastric emptying

to not overwhelm the digestive capacity of the pancreatic enzymes

How does chyme pH effect gastric emptying

HIGH Acidity (Low ph <3.5) slows gastric emptying to allow for adquate neutralization by pancreatic buffers

how does chyme osmolality(when comparing hyper,iso,hypo) effect gastric emptying

rates of emptying are isotonic>hypotonic>hypertonic

what is the physiological significance of slowing gastric emptying

prevent saturation of the duodenal digestive enzymes and minimize large fluctuations of electrolytes in the duodenum

What is the composition of gastric juice

HCL
Pepsin
Gastric Lipase
Mucus
Intrinsic Factor (Essential)

Hydrocholoric Acid in gastric juice (2 fxns)

1)Bacteriocidal agent; when secretion is impaired you see GI infections increase
2)Denaturing Complex polypeptides and works indirectly through pepsin activation from pepsinogen

Pepsin in Gastric Juice

Proteolytic enzyme that initiates protein digestion
Enteropeptidase that works by cleaving interior peptide bonds
initially secreted as pepsinogen

What is pepsinogen to pepsin activation dependent on

pH being less than 3. Depends on HCL secretion.
pepsin itself can also cleave pepsinogen

Are HCL and Pepsinogen essential for protein digestion

No

Gastric lipase in gastric juice

enzyme secreted from the pancreas
contributes significantly to dietary fat digestion

Mucus in gastric juice does what

Lubricates and protects the lining of the lumen from autodeigestion by pepsin

what is the gastric mucosal layer comprised of

Mucus and bicarbonate.
acts to buffer the gastric acid

Intrinsic factor in gastric juice

mucoprotein that binds vit B12 in the stomach, necessary for absorption of B12 in the ileum

What are some fxns of the gastric secretions (3)

1)Digestion of proteins
2) absorption of Vit B12
3)Protection against bacteria and autodigestion by gastric enzymes

Mucus neck cells of the gastric glands

Secrete soluble mucus to mainly lubricate gastric chyme

Surface/superficial epithelial cells of gastric glands

Produce insoluble mucus in response to the chemical (ethanol) or physical irritation (chyme friction)

What is the physical appearance of mucus release by superficial epithelia cells

Visibly thick gel that forms over the mucosal surface

What is the gastric mucosal barrier

Mucosal cells and bicarb secreted from surface cells that neutralizes and protects the mucosa from autodigestion

Parietal cells of the Gastric glands

Produce HCl and intrinsic factor

Peptic chief cells of the gastric glands

produce pepsinogen

APUD cells of the gastric glands

the main site of G cells that produce the hormone gastrin, regulator of gastric acid secretion

In what part of the stomach are parietal (oxyntic) cells located

In the upper 2/3 of the stomach in the fundus and body.

what is the HCl concentration in the gastric lumen and how does it compare to the plasma H+ concentration

It is pH<2 and 10^7 times greater than plasma concentration

What is the mechanism by which H+ and HCO3-
are produced in parietal cells

Use the CO2 produced from normal cell metabolism and make use of carbonic anhydrase to make H+ and bicarb

How is H+ transported into the lumen

Uses an H+/K+ ATPase that pumps H+ across the apical membrane in exhange for a K+

What is the clinical importance of the H+/K+ ATPase channel

Channel is the target of drugs like Omeprazole that prevent excess acid secretion into the lumen.

In what direction of flow of Cl-

It passive diffuses out the apical side of the membrane into the lumen, combines with H+ to make HCl.

What mechanisms in the stomach regulate acid secretion from parietal cells (3)

1)direct neural
2)neuroendocrine
3)paracrine

What is direct neural control of regulation of acid secretion (2)

1)H+ secretion can be increased through P-ANS by the vagus nerve
2)N.T ACh acts through muscurinic receptors

What is neuroendocrine control of regulation of acid secretion

H+ secretion controlled by release of gastrin from pyloric G-Cells which is ultimately controlled by the the stimulation of the vagus nerve.

What is gastrin releasing peptide (GRP)

Neurocrine agent that mediates G-cell stimulation and the release of Gastrin

What is paracrine (neighboring cells) control of regulation of acid secretion

H+ release through H2 receptors stimulated by histamine acitivated by cAMP and adenylyl cyclase

How does histamine secretion compare to other acid secretion control mechanisms

it is independent of both vagus nerve and gastrin stimulation

What is histamine and what cells secrete it

paracrine agent secreted by EnteroChromaffin-Like cells (ECL cells)

What is the clinical significance of the H2 receptors that release histamine and stimulate H+ secretion into the lumen

Targets of drugs like Cimetidine/Pepcid AC that block the H2 receptors, used to control acid secretion by blocking the stimulatory effect of histamine on parietal cells.

How is atropine used to block acid secretion

Atropine works on ECL cell and parietal cells and has a inhibitory effect on ACh receptors

What is gastritis/peptic ulcer disease

Damage to the stomach lumen do to impairment in release of mucus or bircarb by gastric epithelial cells

What factors can reduce the release of mucus and bicarb from gastric epithelia cells and lead to gastritis

Aspirin or other NSAIDS and some alpha-adrenergic agonists.