Digestive System 2 Flashcards
1
Q
Saliva functions
A
1)hydrate oral cavity
2)lubricate food, increases the taste
3)chemical digestion (digestive enzymes)
-salivary amylase for carbs
-linguial lipase for lipids
4)oral hygiene (many enzymes, proteins etc., to fight bacteria, fungi, and caries)
5)anti-microbial
-IgA AB
-cystatins
-histatins
-lysozomes
6)decreases incidence of dental caries
-proline-rich proteins maintain mineralization of teeth
2
Q
Salivary glands 2 groups
A
Extrinsic/major: outside of oral cavity
Intrinsic/minor: inside oral cavity
3
Q
Salivary glands histology
A
1)serous cells:
-watery secretions (enzymes, electrolytes)
-hydrate and clean oral cavity
2)mucous cells:
-viscous secretions (glycoproteins, mucin)
- lubricate food and dissolve food substances so that the taste buds can detect it
4
Q
Extrinsic salivary glands
A
-outside oral cavity
-have ducts to transport saliva into oral cavity
-secret on stimulus:
-mechanoreceptors (chew reflexes)
-chemoreceptors (stimulated by acidic substances
-produce 90% of saliva
Glands:
1) 2 parotid glands
2)2 submandibular glands
3)2 sublingual glands
Histology: serous and mucous
5
Q
Intrinsic salivary glands
A
-inside oral cavity
-no ducts
-constantly secreting saliva
-produce 10% of total saliva
-buccal glands
-labial glands
-palatine glands
Histology: mucous
6
Q
Parotid gland location
A
-anterior to ear
-between master muscle and skin
7
Q
Partotid duct
A
“Stensen duct”
Pierces muscles
Empties into oral cavity at the level of second maxillary/upper molar
8
Q
Parotid gland histology
A
Serous
9
Q
Parotid gland histology
A
Serous
10
Q
Submandibular gland location
A
-inner medial surface of mandibular body
-on digastric triangle
11
Q
Submandibular duct
A
“Warthon’s duct”
Empties into oral cavity near lingual frenulum
12
Q
Submandibular gland histology
A
Serous and mucous cells
13
Q
Sublingual gland location
A
Underneath tongue
14
Q
Sublingual duct
A
“Ducts of Rivinus”
10-20 ducts empty into floor of oral cavity
15
Q
Sublingual gland histology
A
Mucous cells
16
Q
Innervation of salivary glands
A
By PNS: CN 7 and CN 9
➡️increase volume of saliva
➡️water and electrolyte-rich
17
Q
Pathway for submandibular and sublingual gland
A
Location: brain stem (pons)
Nucleus: superior salivatory nucleus (part of facial nerve CN7- PNS)
➡️fibers exist at pontomedullary junction
➡️exit cranial cavity through internal acoustic meatus
➡️transverse through bony canal in the medial and posterior wall of middle ear cavity
➡️exit canal, move anteriorly as chorda tympani
➡️chorda tympani combines lingual nerve (from trigeminal nerve CN5)
➡️synapse at submandibular ganglion
➡️from this point: postgamglionic PNS fibers
➡️innervate sublingual and submandibular salivary gland
18
Q
Pathway for parotid gland
A
Location: brain stem (pons)
Nucleus: inferior salivary nucleus(part of glossopharygeal nerve CN9-PNS)
➡️fibers pass through jugular foramen
➡️enters middle ear cavity through tympanic canaliculus
➡️go to promontory (on the medial wall of middle ear cavity), give off branches
➡️continues as lesser petrosal fossa
➡️pass through hiatus of lesser petrosal nerve in middle cranial fossa
➡️exit middle cranial fossa through foramen ovale (together with mandibular part of trigeminal nerve)
➡️continues down otic ganglion
➡️synapses on postganlionic cell bodies of parasympathetic motor fibers
➡️postganglionic PNS motor fiber innervate parotid gland
19
Q
Afferent stumuli of salivary glands:
How do these fibers know when to fire?
A
-inside oral cavity: special receptors (on tongue, in cheeks, around tonsils, in pharyngeal area, etc.)
-chemoreceptors: react to acidic
-mechanoreceptor: react to chewing
➡️stimulates superior and inferior salviatory nucleus
➡️activates motor fiber to send stimulus for salivation
Other stimuli: sight, smell, thought
20
Q
Efferent pathways- SNS of salivtory glands
A
-by SNS: viscous protein-rich saliva
-from T1-T4, SNs fibers go up to head and neck region
➡️go to superior cervical ganglia
➡️give off fibers wrapping around carotid artery: carotid plexus
➡️continues as deep petrosal nerve to the ptyergoid canal
➡️to pterygopalatine fossa
➡️supply glands (extrinsic glands)
21
Q
Acinus structure
A
Sack-like region
Lined by acinar cells
22
Q
Structure of duct of salivary gland
A
-different types (striated, interlobular, intercalated, excretory duct)
-lined w/ ductal cells
23
Q
Acinar cells membrane
A
Basolateral + apical
24
Q
Saliva production mechanism: transporters
A
-distributed throughout membranes
-basolateral membrane:
➡️transport substances into cell
-pump:2K+ in, 3Na+ out
-pump: Na+ K+ 2Cl- in
-Aquorin 3: H2O in
-Apical membrane:
➡️transport substances out of the cell (into the lumen of acinus)
-pump: K+out, H+ in
-pump: HCO3- out, Cl- in
CFTR (cystic fibrosis transmebrane receptor protein) Cl- out
-Aquoporin 5: water
25
Mechanism of saliva activation: components of the lumen
-Na+: into lumen: mainly by paracellular transport
-K+: into cell: Na/K-pump , Na/K/2Cl pump
Into lumen: by K/H-pump, leakage channels
-Cl-: into cell: Na/K/2Cl-pump
Into lumen: CFTR
-HCO3-: into cell: CO2 +H2O➡️H2CO3 by carbonic anhydrase
-Ca2+, PO4-3
-H2O: into cell: aquaporin 3
Into lumen: paracellular transport, aquaporin 5
26
Saliva production mechanism: primary saliva
-in lumen of acinus
-Na+ and Cl- the amount in acinus is equal to amount of water
➡️isotonic to blood plasma
27
Saliva production mechanism: secondary saliva
- in the lumen of the duct
-primary saliva modified
-Na+ pumped into ductal cells by Na/H pump
-Cl- pumped into ductal cells by Cl-/HCO3- pump
-amount of Na+, Cl- is now less than water
➡️hypotonic to blood plasma
28
Salivatory glands: effect of ANS
-🩸 supply to glands
-it can help determine the amount of saliva produced
-PNS releases AcH
-SNS releases NE
-NE stimulates vasoconstriction blood flow
-⬇️🩸 flow
-⬇️ electrolyte and water secretion
29
Salivatory glands: effects of PNS
-AcH binds on muscarinic receptors M3
➡️activates Gq protein (uses GTP)
➡️stimulates phospholipase C (PLC)
➡️breaks down PIP2 into DAG and IP3
➡️IP3 stimulates Ca release inside cell
➡️Ca stimulates PKC (protein kinase C) and CAM kinases
➡️phosphorylation of channels
➡️⬆️release: H2O, Na, HCO3- (electrolyte)
30
salivatory gland: effects of SNS
-NE binds to B receptor
➡️activate Gs protein (uses GTP)
➡️activates Adenylate cyclase➡️cAMP
➡️PKA stimulates executors of secretory ganules (filled with/proteins, enzymes,…)
➡️⬆️releases: mucin, salivatory amylase
31
Deglutition
Swallowing-bring food from oral cavity to stomach
32
Path of food: swallowing
Oral cavity ➡️pharynx➡️esophagus ➡️stomach➡️duodenum:absorption
33
Oral/buccal phase (1) receiving food)
-bring food into oral cavity
- for eating, we need to open mouth
➡️bring mandibule down
➡️by mandibular depressor muscles
-we need to depress mandible
➡️stretches the antagonist muscles (elevators)
➡️stretch activate muscle spindles (proprietors)
➡️activates afferent fibers of CN 5
➡️sends info to brainstem
➡️activates motor fibers of CN 5
➡️elevation of Mn
34
Buccal phase (2) turning food into bolus)
-mechanical digestion= breaking food into small pieces (not breaking chemical bonds
-muscles of mastication
-teeth:
-incisors: cutting food
-canines: tearing food
-molars: grinding, crushing food
Once muscles contract, pressure receptors detect it (in oral mucosa, gingiva, tongue,…)
➡️activates sensory nerves
➡️inhibit trigeminal nerve
➡️chewing stops
-salivary glands
-muscles + teeth broke food down into small particles
-saliva lubricates particles
-moisten, lubricate, soften it
Mucins, digestive enzymes mix with it
➡️mass of food= bolus
Mastication+saliva:
-⬆️ surface area for chemical digestion (salivary amylase, lingual lipase)
⬇️ abrasion of GI lining (especially pharynx and esophagus)
35
Buccal phase (3) role of tongue)
Tongue takes special shape and position:
-intrinsic muscles:
-form central trough around food bolus
-extrinsic muscles:
-elevate tongue so that lip touches palate
➡️creates downward slope towards pharynx
➡️bolus can now slide right into pharynx
36
Pharyngeal phase
-once bolus touches palatoglossal arch➡️ oral phase ends, pharyngeal phase begins
-in back or oral cavity we find:
-palatopharyngeal arch
-palatoglossal arch
-tonsillar fossa
-bolus touches these areas:
➡️many sensory receptors located around these areas
➡️activates afferent fibers of glossopharyngeal nerve (CN9)
➡️stimulus passes ganglion, goes to brainstem (nucleus ambiguous)
➡️activates vagus nerve (CN 10)
-from oral cavity bolus continues to:
-nasopharyxn
-esophagus
-larynx
37
How do we prevent the bolus from going to the nasopharynx?
-bolus stimulates sensory afferent fibers of CN9
➡️activates efferent fibers CN10
-contracts uvula➡️elevates uvula
➡️closes nasopharynx
-contracts muscles of soft palate➡️elevates soft palate➡️⬆️distance between bolus and soft palate
➡️activates efferent fibers of CN V3
-contracts muscles supporting soft palate➡️ tenses soft palate➡️ supports elevation of soft palate
38
How do we prevent the bolus from going to larynx?
-when we swallow 2 things happen:
1)approximate/adducts vocal cords
-true vocal cords: important to phonation (vibrate➡️ create sound)
-contraction of muscles
➡️space between vocal cords (glottis) shrinks
2)epiglottis
-retroversion of epiglottis:
-when bolus touches epiglottis, it bends over the glottis to protect it (close it)
-Contraction of muscle
➡️pull aryepilglottic folds together
➡️bolus is diverted from larynx
39
How to ensure that pharynx is ready for bolus?
-arches contract:
➡️palatoglossal and palatopharyngeal arches tighten (to ensure that only small particles continue into pharynx, not big pieces)
-elevate pharynx, elevate larynx➡️ bring pharynx closer to bolus
-out longitudinal layer of muscles contract
-squeeze pharynx(to push bolus downward)
-contraction➡️ pull hyoid bone up➡️ pulls larynx up and anteriorly
-bolus moves into oesophagus:
-at the lowest part of inferior pharyngeal constrictor muscle acts as upper esophageal sphincter (UES) (CN10)
-pharyngeal peristalsis ➡️ descending axons relax
➡️UES relaxes
➡️bolus can be received (larynx was moved out of the way (anteriorly + up)➡️ enough place for esophagus to receive bolus
40
Esophageal phase:
-begins when bolus moves past UES
-esophagus is very muscular
-peristalsis started in pharynx, continues in esophagus
➡️descending axons relax
➡️LED relaxes (lower esophageal sphincter/ cardiac sphincter)
➡️bolus arrives in stomach and can further be digested by gastric acids and other enzymes
-problems w/ relaxation of LES:
-GERD(esophagus passes through diaphragm)
-hiatal hernia(b/c esophagus passes through diaphragm)
41
Esophageal phase: primary Peristalsis
-continuation of pharyngeal peristalsis
➡️like a wave starting at pharyngeal constrictor going all the way down the esophagus (CN 10)
➡️LES relaxes
42
Esophageal phase: secondary peristalsis
-when bolus is stuck
➡️stretches esophageal walls
➡️activates stretch receptors
-above bolus:
-stimulates circular layer of muscles
-inhibits longitudinal layer of muscles
-below bolus, descending axons:
-stimulates longitudinal layers of muscles
-inhibits circular layers of muscles
➡️contract above and relax below bolus to ensure it moves down
43
Esophageal phase: secondary peristalsis
-when bolus is stuck
➡️stretches esophageal walls
➡️activates stretch receptors
-above bolus:
-stimulates circular layer of muscles
-inhibits longitudinal layer of muscles
-below bolus, descending axons:
-stimulates longitudinal layers of muscles
-inhibits circular layers of muscles
➡️contract above and relax below bolus to ensure it moves down
44
Gastric secretion: cephalic and gastric phase: mechanism of hydrochloric acid production
-there is a lot of mitochondria in the parietal cells which makes them oxygen dependent
-as a result of cellular respiration, carbon dioxide will be produced
➡️CO2 when combines with water the presence of carbonic anhydrase enzyme
➡️carbonic acid dissociates into protons and bicarbonate
-protons will go to the lumen through the proton pump
-bicarbonate will go out into the blood vessels such as the gastric veins, making the🩸 more alkali than gastric artery
-this is referred to as alkaline tide
45
Gastric secretion: cephalic and gastric phase: mechanism of hydrochloric acid production part 2
-since HCO3-, leaves parietal cells, another (-) ion must come into the cell, which is Cl-
-the Cl- will travel through the parietal cell only to be pushed out to the lumen through special channels
-now, in the lumen, there’s H+ and Cl-➡️HCl
-on the cell membrane, there’s Na/K ATPase which pumps 3Na+ out of cell and 2K+ into cell
➡️K+ that was pumped into the cell can drain out of the cell into lumen passively. As a result, it is going to be pumped back into cell through proton/K+ pump
-omeprazole: competitive inhibitor of proton/K+ pump➡️inhibits gastric acid secretion
-when there is a lot of protons in the
cell, some of the protons will be pushed out and the Na+ that was pushed out will be going into the cell
-this prevents excessive protons in the cell which can make cell very acidic
46
Why is protective mechanism of stomach important?
HCl and proteolytic enzyme pepsin are very corrosive and can even damage epithelial cells of the stomach
47
Mucosal barrier
-prevents corrosion of the stomach
-defects in the barrier contribute to the erosions that may happen in a peptic ulcer
48
Mucous cells of mucosal barrier
These cells in the stomach secrete molecules that form mucosal barrier. The cells include:
-foveolar cells
-mucous neck cells
49
Secretory molecules of mucosal barrier
Barrier made up of:
-water (95%)
-electrolytes
- Na+
-K+
-phospholipids
-mucin proteins
-it is the most important
-forms the thick mucosal barrier
-HCO3-
-closer to the apical surface of the cells
50
Cephalic phase
-no food in stomach
-gastric juice is produced before the food enters the stomach to prepare for the food
51
Cephalic phase: stimulus
Sight
Smell
Thought
Taste of food
52
Cephalic phase: taste bud stimulus
-taste buds picks up different types of chemicals➡️sends the info down the cranial nerves
53
How does gastric stimuli influence gastric secretion?
-stimulation of cerebral cortex neurons
➡️sends info down the hypothalamus
➡️hypothalamus sends descending axons downwards to dorsal nucleus of vagus in the medulla
➡️vagus nerve goes to all parts of stomach
-vagus nerve stimulates partietal and chief cells to make HCl and pepsinogen➡️pepsinogen at optimal pH 1.8-3.5 can be activated to a digestive enzyme: pepsin
54
Cephalic phase: inhibition
-anything that activates CNS
55
Gastric phase
Food is already in the stomach
56
Gastric phase: distension stimulus (vagovagal reflex)
-long reflex arc
-stretch receptors are coupledw/ afferent fibers of CN10 which is a sensory nerve
➡️sends signals to NS
-efferent nerves which reach the stomach sends signals away from NS
-stretching of the stomach stimulates CN10
➡️stimulation of parietal and chief cells
➡️triggers HCl production and pepsin secretion
57
Gastric phase: distension stimulus (submucosal plexus)
-short reflex arc
-submucosal plexus, which are neuron in submucosa can stimulate different types of cells of the stomach ➡️this includes parietal and chief cells➡️ this then ⬆️ HCl and pepsin production
58
Gastric phase: distension stimulus (myenteric plexus)
-short reflex
-concerns w/ contractibility and motility of stomach
59
Gastric phase: partially digested proteins
-directly related to pH
-proteins are buffers
-AA make up proteins w/ (-) charges that can tie up protons
-when there’s a lot of proteins
➡️pH-initially low (a lot of protons)
➡️⬆️pH
➡️inhibit conversion of pepsinogen into pepsin
-G cells in gastric glands of atrum ➡️responds to partially digested proteins
-⬆️ partially digestive proteins in gastric mucosa stimulated G cells➡️secretes gastrin➡️travels through🩸
60
Gastric phase: partially digested proteins (it reaches parietal cells)
-bind to CCK 2 receptor
➡️⬆️incracellular Ca2+ via GQ pathway
➡️stimulate proton pump on parietal cell
➡️pushes H+ out of lumen and bring K+ into lumen
➡️environment becomes concentrated w/ protons (acidic)- component of HCl
61
Parietal cells
Secrete HCl
Secrete intrinsic factors
Absorb Vit B12
62
Gastric phase: partially digested proteins stimulus (reaches chief cell)
-found throughout stomach
-gastrin binds onto CCK 1 receptor of chief cell
➡️stimulate vescicles in chief cell to fuse with/ cell membrane
➡️exocytosis w/ pepsinogen
-pepsinogen can be converted to pepsin (active proteolytic form)
-at N-terminus peptide, there’s a specific sequence in which when there’s a proper concentration of protons, pH1.8-3.5 (optimal) stimulates conversion of pepsinogen to pepsin
-HCl needed to activate
63
Gastric phase inhibition
-SNS
-somatostatin
-stimulus:
-really low pH in lumen of stomach
➡️high amounts of HCl
-mechanism:
-antral D cells detects high concentration of the proton
➡️secretes somatostatin in 🩸
➡️somatostatin acts on nearby parietal cells
➡️binds to somatostatin receptors on antrum
➡️inhibits G cells from releasing gastrin
-gastrin that was initially responsible for stimulation of pepsin and H+ secretion will be inhibited
➡️high amounts of HCl in stomach with be lowered
64
Gastric phase: control of antral cells of stomach
-vagus nerve can directly act on D and G cells
-Dcells release stomatostatin(inhibitory)
-g cells release gastrin which ⬆️ pepsin and HCl secretion
65
Gastric phase: D cells
-AcH (PNS), which is released by CN10 binds to M3 receptor on D cells
➡️inhibits D cells from releasing somatostatin
➡️⬆️ in pepsin and HCl secretion
-gastrin can also inhibit D cells from releasing somatostatin by binding to CCK2 receptor
66
Gastric phase: G cells
-Gastrin releasing peptide (GRP)- bombesin molecule (also release by CN10) can also bind to receptor on G cell and stimulate it
➡️⬆️ gastrin release
➡️⬆️ pepsin and HCl secretion
67
Gastric phase: control of parietal cells (of corpus)- gastrin
- binds to CCK2 receptor
➡️⬆️ intracellular Ca2+ via GQ pathway
➡️stimulate proton pump on parietal cells
➡️pushes protons out of lumen and bring K+ into cell
➡️environment becomes concentrated w/ protons (acidic)
68
Gastric phase: control of parietal cells (of corpus)-AcH
-binds to M3 receptors
➡️⬆️Ca2+ level intracellularly via GQ pathway
➡️stimulate proton pump
69
Gastric phase: control of parietal cell (of corpus)- histamine
-binds to H2 receptor
➡️acts on GS pathway
➡️stimulate HCl secretion
70
Gastric phase: control of parietal cells (of corpus)- prostaglandin
-PGE2 binds to EP3 receptor
➡️acts on GInhib pathway
➡️inhibit HCl pathway
71
Gastric phase: control of parietal cells (of corpus)- somatostatin
-binds to SST receptor
➡️enter the cell and act through Ginhib pathway
➡️inhibits proton pump directly
72
Gastric phase: control of chief cells (of corpus)- gastrin
-binds to CCk1 receptor on chief cell➡️ stimulate vescicles in chief cell to fuse with cell membrane➡️ excytosis w/ pepsinogen
73
Gastric phase: control of chief cells (of corpus)- histamine
-binds to H2 receptor
➡️stimulate GS pathway
➡️⬆️ pepsinogen release
74
Gastric phase: control of chief cells (of corpus)- AcH
-binds to M3 receptor➡️⬆️ intracellular Ca2+ concentration ➡️ stimulate pepsinogen secretion
75
Gastric phase: control of chief cells (of corpus)- secretin
-secreted from S cells of duodenum which responds to acidic and fatty chyme
-stimulate through an unknown mechanism which helps with release of pepsinogen
76
Gastric phase: control of enterochromaffin like cells (ECL) (of corpus)- AcH
Bind to M3 receptor➡️stimulate release of HCl
77
Gastric phase: control of ECL (of corpus)- gastrin
Help stimulate release of histamine
78
Gastric phase: control of ECL (of corpus)- somatostatin
-comes from D cells of corpus, not the antral D cells
-inhibits release of histamine
79
Gastric phase: Control of D cells (of corpus)
Stimulation of M3 receptor which is specifically sensitive to AcH
➡️inhibits D cells
➡️inhibits release of somatostatin
➡️prevents ECL cells from being inhibited
➡️stimulates histamine release
80
basic motility of stomach
When stomach contracts it produces 3 strong peristatic contraction starting at the cardia ➡️moves down fundus ➡️antrum➡️and reach pylorus, where waves are strongest
-pushes 25% of chyme back into corpus (retropulsion)➡️to continue mixing the chyme w/ HCl and pepsin
-some gets chemically digested
-others are digested mechanically later on
-pushes approximately 3ml of chyme out into duodenum
-amount lets duodenum be ready and makes modifications when needed
-this also prevents damage to duodenal lining due to high proton concentration of strong stomach chyme
81
Contents of chyme
-glucose
-protons
-partially digested peptides
-Fatty acid
82
Intestinal phase: stimulatory factors- partially digested proteins
-acts through the release of intestinal gastrin (G34)
-when the chyme reaches duodenum:
➡️high concentration of partially digested proteins (peptones) stimulates the duodenal G cells
➡️release of intestinal gastrin (G34)
➡️gastrin, like a hormone, moves through the 🩸
➡️reaches parietal/oxyntic cell in the corpus
83
Intestinal phase: stimulus from partially digested peptides- parietal cells
Gastrin binds to receptors on parietal cell
➡️stimulate parietal cell through signaling mechanisms
➡️activate H/K ATPase
➡️proton pump pushes protons and brings in K+
84
Intestinal phase: partially digested peptides stimulus- chief cells
Gastrin also has receptors on chief cell➡️binds to receptor➡️stimulates vescicles in chief cell to fuse with cell membrane➡️ contents of vescicles: pepsinogen, will be released in lumen of stomach
-pepsinogen can be converted to pepsin at pH 1.8-3.5
-pepsin is a protein digesting enzyme
85
Pepsinogen➡️pepsin
-pepsinogen➡️pepsin: 1.8-3.5
-pepsin-pepsinogen: greater than 3.5
-pH higher than 7.2 creates irreversible inactivation of pepsinogen
More acidic environment➡️higher the conversion of pepsinogen to pepsin➡️more the proteins will be digested
But very acidic environment can inhibit secretion of HCl➡️ inhibit conversion of pepsinogen to pepsin
86
Intestinal phase: entero-oxyntin
⬆️concentration of peptones
Stimulate different types of endocrine cells
➡️release unknown chemicals-entero-oxytnin
➡️circulates through 🩸
➡️reach parietal cells via stimulators pathways
➡️stimulate special receptor on parietal cells which stimulate HCl secretion
87
Intestinal phase: secretin stumuli
Stimulates chief cells to make pepsinogen
88
Intestinal phase: inhibitiontory factor- secretin
-secreted by S cells
-S cells release secretin in response to:
⬆️ concentration of protons
⬆️ concentration of fats (FA)
89
Functions of secretin in the stomach
-inhibits gastric acid secretion
-mechanism:
-secretin travels through 🩸 vessels reaching antral G cells of the stomach➡️ bind to receptors on G cells➡️inhibit G cells➡️ release of gastrin will be inhibited➡️ HCl secretion will be inhibited
90
Functions of secretin in the liver
-stimulates liver to make bile
-mechanism:
-secretin travels to liver
➡️binds to receptor on the liver
➡️stimulate hepatocytes to convert any cholesterol into bile acids (main component of bile that helps emulsify fats)
➡️⬆️bile synthesis
➡️⬆️ concentration of bile acids
➡️bile drains into common hepatic ducts
➡️passes through common hepatic duct which joins cystic duct of gallbladder, forming the common bile duct
➡️common bile duct fuses with main pancreatic duct forming the hepatopancreatic ampulla
➡️sphincter of oddi muscle/hepatopancreatic sphincter which wraps around ampulla relaxes to release bile into duodenum
➡️bile reacts with FA and emulsify it
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Bile contents
-bile acids and salts
-phospholipid
-cholesterol
-pigments
-water
-electrolyte chemicals
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Functions of secretin in the liver
-secretin responds to acidic chyme
-stimulates ductal epithelial cells to make HCO3-
-mechanism:
-Secretin binds to the receptor on acinar ductal epithelial cells
➡️stimulate it to release HCO3- (basic substance)
➡️react to protons in the chyme to neutralize it
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Intestinal phase: inhibiory factor- CCk
Release by entero-endocrine I cells which is stimulated by high concentration of:
-FA (fatty chyme)
-partially digested proteins
-oligosaccharides (hyperosmolar chyme)
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Function of CCK in the stomach
-inhibits release of HCl
-duodenum is filled with partially digested substances➡️so slowing the acid secretion slows down emptying of the stomach
-high proton concentration in the chyme can also damage the duodenal lining causing ulcers
Mechanism:
-CCK goes into the🩸 to reach parietal cells of stomach
➡️bind the receptor on the parietal cells
➡️inhibit the proton pump via Ginhib pathway
➡️inhibits release of HCl
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Functions of CCK in the liver
-binding of CCK to the receptor on the liver accentuates the action of secretin
-this ⬆️bile synthesis➡️which ⬆️ the concentration of bile acids➡️bile acids react with FA and emulsify it➡️this helps with digestion and absorption of fat
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Functions of CCK in the gallbladder
-cause gallbladder contractions and relaxes sphincter of Oddi
-mechanism:
-binds to receptor on gallbladder➡️gallbladder contracts➡️squeeze out any concentrated bile➡️CCK binds itself to the receptor on the sphincter of Oddi➡️and stimulates the sphincter and relaxes it➡️bile will be released into duodenal mucosa
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How does gallbladder help with concentrating bile?
By getting rid of a lot of water and electrolytes
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Functions of CCK in the pancrea
-CCK stimulate acinar cells to release digestive enzymes
-acinar cells in the acini are concentrated with granules which are rich in different types of digestive enzymes:
-pancreatic proteases
-trypsin
-chymotrypsin
-carboxy peptidase
-helps with digestion and absorption of proteins
-pancreatic amylase
-help in digestion of FA
-pancreatic nuclease
-mechanism:
-CCK binds to receptors of acinar cells and stimulate fusion of vescicles with cell membrane (exocytosis)
-enzymes are precursors- they are inactive and needs to undergo certain chemical reactions in the duodenum to be activated
-importance: active form can react with epithelial cells of pancreas, digesting it is as what may happen in pancreatitis
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Intestinal phase: inhibitory factory- peptide YYa d neurotensin chemicals
-released by different types of endocrine cells
-endocrine cells are activated by stretch
-mechanism:
-a lot of chyme in the intestine ➡️ distension of wall➡️ activate different endocrine cells➡️ release peptide YY and neurotensin➡️ moves through🩸➡️acts on receptors present on parietal cells➡️inhibit H/k ATPase via signaling pathway➡️less HCl production
-this prevents excessive release of acidic chyme into duodenum
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Intestinal phase: inhibitory factor- gastric inhibitory peptide (GIP) chemical
-Also known as “glucose-dependent insulinotropic peptide”
-Released by enteroendocrine K-cells which responds to
high concentrations of oligosaccharides/polysaccharides and fats
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Functions of GIP in the stomach
-Inhibit gastric secretion
-Mechanism:
-Travels through the blood to reach the parietal cells
→ bind to the GIP receptors on the parietal cells → triggers intracellular inhibitory signals → inhibits the parietal cells from releasing hydrochloric acids
-Inhibit GI emptying
-Inhibiting the chyme from entering the duodenum
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Functions of GIP in the pancreas
-Stimulate insulin release
-Mechanism:
-Islets of Langerhans contains: Alpha cells
-Delta cells
-Polypeptide cells
-F cells
-Beta cells
-Contain receptors which are sensitive to glucose
-Insulinotropic peptide/gastric inhibitory peptide
-Stimulate the release of insulin
-Insulin is primarily responsible to decrease
blood glucose levels
-Primarily released during feeding/fed state
-This helps in increase in glucose and amino acids uptake → increase glycogenesis, lipogenesis and protein synthesis
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Intestinal phase: inhibitory factors- AcH
Released by the vagus nerve (cranial nerve X) from the central nervous system
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Functions of AcH in the pancreas
-Stimulate insulin release
-Mechanism:
-Acetylcholine released → bind to the muscarinic receptors of the pancreatic beta cells → stimulate the beta cells to release insulin
-Relaxes the sphincter of Oddi by binding to the receptors on the sphincter
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Functions of AcH in gallbladder
Bind to the receptors in the gallbladder → help in gallbladder contractions
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Intestinal phase: inhibitory factors- chemoreceptors
-Activated by the high concentration of protons
-Remember:
-Vagus nerve have fibers that reach the parietal cells→ parietal cells are very sensitive to acetylcholine (strongest stimulus) → acetylcholine that act on the parietal cells stimulate the hydrochloric acid secretion
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Intestinal phase: chemoreceptors- inhibition of parasympathetic outflow
High concentration of protons may destroy the duodenal lining → the chemoreceptors detect the high concentration of protons → inhibit the vagus nerve → decrease the hydrochloric acid secretion
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Intestinal phase: chemoreceptors- stimulation of sympathetic outflow
-chemoreceptors fibers stimulate paravertebral ganglion
➡️⬆️APs of post ganglion’s nerve
➡️act on alpha 1adenergic receptors on pylorus sphincter
➡️sphincter contracts and squeezes
➡️prevent the chyme to be released into duodenum
➡️prevent damage to the duodenum from high concentration of protons in the chyme
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Protective mechanism of the stomach
-The proton concentration in the stomach is 100,000 times more concentrated than in the blood
-The mucosal barrier protects the stomach from being digested by this very acidic environment
-The barrier is consisted of:
-mucus gel layer
-HCO3-
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Mucus gel layer of mucosal barrier
Located at the top, which made up of: -Water (95%)
-Electrolytes
-Sodium
-Potassium
-Phospholipids
-Mucin proteins
-it is the most important
-Increase the viscosity and forms the thick
mucosal barrier
-Prevents the proton from damaging the
epithelial layer
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HCO3- of mucosal barrier
High concentration of bicarbonate at the bottom
-Basic substance
-Right above the mucosal cells
-If the pepsin secretion starts rising and tries to move through the gel layer, the bicarbonate will inhibit the pepsin and turns it into the pepsinogen
-If the protons by chance penetrate through the gel layer → it will combine with bicarbonate → forming carbonic acid → carbonic acid breaks down into carbon dioxide (the burping gas) and water
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Mucosa subdivisions
-epithelium
-lamina propria
-muscularis mucosae
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Mucosa- epithelium subdivision: tissue type
Stratified squamous epithelium in the mouth, oropharynx, laryngopharynx, esophagus, and anus
Simple columnar epithelium in the remainder of the canal
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Mucosa- lamina propria subdivision tissue type
Areolar connective tissue w/ blood vessels
Many lymphoid follicles, especially at tonsils and mucosa-associated lymphoid tissue (MALT)
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Mucosa- muscularis mucosae subdivision: tissue type
Thin layer of smooth muscle
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Functions of mucosa
-secretion of mucus, digestive enzymes, and hormones
-absorption of end products into the 🩸
-protection against infectious disease
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Submucosa tissue type
Areolar and dense irregular connective tissue containing blood vessels, lymphatic vessels, and nerve fibers (sub mucosal nerve plexus)
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Submucosa functions
🩸 vessels absorb and transport nutrients
Elastic fibers help maintain the shape of each organ
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Muscularis externa subdivision of layers
-circular layer- liner layer of smooth muscle
-longitudinal layer- outer layer of smooth muscle
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Functions of muscularis externa
Segmentation and peristalsis of digested food along the tract are regulated by meyenteric nerve plexus
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Serosa (visceral peritoneum) subdivision of layer
-connective tissue: Areolar connective tissue
-epithelium (mesothelium): simple squamous epithelium
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Serosa function
Reduces friction as the digestive system organs slide across one another
