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A&p2 > Digestive System 2 > Flashcards

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

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2
Q

Salivary glands 2 groups

A

Extrinsic/major: outside of oral cavity

Intrinsic/minor: inside oral cavity

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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

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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

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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

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6
Q

Parotid gland location

A

-anterior to ear
-between master muscle and skin

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7
Q

Partotid duct

A

“Stensen duct”

Pierces muscles

Empties into oral cavity at the level of second maxillary/upper molar

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8
Q

Parotid gland histology

A

Serous

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9
Q

Parotid gland histology

A

Serous

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10
Q

Submandibular gland location

A

-inner medial surface of mandibular body
-on digastric triangle

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11
Q

Submandibular duct

A

“Warthon’s duct”

Empties into oral cavity near lingual frenulum

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12
Q

Submandibular gland histology

A

Serous and mucous cells

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13
Q

Sublingual gland location

A

Underneath tongue

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14
Q

Sublingual duct

A

“Ducts of Rivinus”

10-20 ducts empty into floor of oral cavity

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15
Q

Sublingual gland histology

A

Mucous cells

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16
Q

Innervation of salivary glands

A

By PNS: CN 7 and CN 9
➡️increase volume of saliva
➡️water and electrolyte-rich

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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

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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

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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

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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)

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21
Q

Acinus structure

A

Sack-like region

Lined by acinar cells

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22
Q

Structure of duct of salivary gland

A

-different types (striated, interlobular, intercalated, excretory duct)
-lined w/ ductal cells

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23
Q

Acinar cells membrane

A

Basolateral + apical

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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

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25
Q

Mechanism of saliva activation: components of the lumen

A

-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

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26
Q

Saliva production mechanism: primary saliva

A

-in lumen of acinus
-Na+ and Cl- the amount in acinus is equal to amount of water
➡️isotonic to blood plasma

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27
Q

Saliva production mechanism: secondary saliva

A
  • 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
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28
Q

Salivatory glands: effect of ANS

A

-🩸 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

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29
Q

Salivatory glands: effects of PNS

A

-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)

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30
Q

salivatory gland: effects of SNS

A

-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

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31
Q

Deglutition

A

Swallowing-bring food from oral cavity to stomach

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32
Q

Path of food: swallowing

A

Oral cavity ➡️pharynx➡️esophagus ➡️stomach➡️duodenum:absorption

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33
Q

Oral/buccal phase (1) receiving food)

A

-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

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34
Q

Buccal phase (2) turning food into bolus)

A

-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)

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35
Q

Buccal phase (3) role of tongue)

A

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

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36
Q

Pharyngeal phase

A

-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

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37
Q

How do we prevent the bolus from going to the nasopharynx?

A

-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

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38
Q

How do we prevent the bolus from going to larynx?

A

-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

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39
Q

How to ensure that pharynx is ready for bolus?

A

-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

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40
Q

Esophageal phase:

A

-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)

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41
Q

Esophageal phase: primary Peristalsis

A

-continuation of pharyngeal peristalsis
➡️like a wave starting at pharyngeal constrictor going all the way down the esophagus (CN 10)
➡️LES relaxes

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42
Q

Esophageal phase: secondary peristalsis

A

-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

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43
Q

Esophageal phase: secondary peristalsis

A

-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

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44
Q

Gastric secretion: cephalic and gastric phase: mechanism of hydrochloric acid production

A

-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

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45
Q

Gastric secretion: cephalic and gastric phase: mechanism of hydrochloric acid production part 2

A

-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

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46
Q

Why is protective mechanism of stomach important?

A

HCl and proteolytic enzyme pepsin are very corrosive and can even damage epithelial cells of the stomach

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47
Q

Mucosal barrier

A

-prevents corrosion of the stomach
-defects in the barrier contribute to the erosions that may happen in a peptic ulcer

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48
Q

Mucous cells of mucosal barrier

A

These cells in the stomach secrete molecules that form mucosal barrier. The cells include:
-foveolar cells
-mucous neck cells

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49
Q

Secretory molecules of mucosal barrier

A

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
Q

Cephalic phase

A

-no food in stomach
-gastric juice is produced before the food enters the stomach to prepare for the food

51
Q

Cephalic phase: stimulus

A

Sight
Smell
Thought
Taste of food

52
Q

Cephalic phase: taste bud stimulus

A

-taste buds picks up different types of chemicals➡️sends the info down the cranial nerves

53
Q

How does gastric stimuli influence gastric secretion?

A

-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
Q

Cephalic phase: inhibition

A

-anything that activates CNS

55
Q

Gastric phase

A

Food is already in the stomach

56
Q

Gastric phase: distension stimulus (vagovagal reflex)

A

-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
Q

Gastric phase: distension stimulus (submucosal plexus)

A

-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
Q

Gastric phase: distension stimulus (myenteric plexus)

A

-short reflex
-concerns w/ contractibility and motility of stomach

59
Q

Gastric phase: partially digested proteins

A

-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
Q

Gastric phase: partially digested proteins (it reaches parietal cells)

A

-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
Q

Parietal cells

A

Secrete HCl
Secrete intrinsic factors

Absorb Vit B12

62
Q

Gastric phase: partially digested proteins stimulus (reaches chief cell)

A

-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
Q

Gastric phase inhibition

A

-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
Q

Gastric phase: control of antral cells of stomach

A

-vagus nerve can directly act on D and G cells
-Dcells release stomatostatin(inhibitory)
-g cells release gastrin which ⬆️ pepsin and HCl secretion

65
Q

Gastric phase: D cells

A

-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
Q

Gastric phase: G cells

A

-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
Q

Gastric phase: control of parietal cells (of corpus)- gastrin

A
  • 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
Q

Gastric phase: control of parietal cells (of corpus)-AcH

A

-binds to M3 receptors
➡️⬆️Ca2+ level intracellularly via GQ pathway
➡️stimulate proton pump

69
Q

Gastric phase: control of parietal cell (of corpus)- histamine

A

-binds to H2 receptor
➡️acts on GS pathway
➡️stimulate HCl secretion

70
Q

Gastric phase: control of parietal cells (of corpus)- prostaglandin

A

-PGE2 binds to EP3 receptor
➡️acts on GInhib pathway
➡️inhibit HCl pathway

71
Q

Gastric phase: control of parietal cells (of corpus)- somatostatin

A

-binds to SST receptor
➡️enter the cell and act through Ginhib pathway
➡️inhibits proton pump directly

72
Q

Gastric phase: control of chief cells (of corpus)- gastrin

A

-binds to CCk1 receptor on chief cell➡️ stimulate vescicles in chief cell to fuse with cell membrane➡️ excytosis w/ pepsinogen

73
Q

Gastric phase: control of chief cells (of corpus)- histamine

A

-binds to H2 receptor
➡️stimulate GS pathway
➡️⬆️ pepsinogen release

74
Q

Gastric phase: control of chief cells (of corpus)- AcH

A

-binds to M3 receptor➡️⬆️ intracellular Ca2+ concentration ➡️ stimulate pepsinogen secretion

75
Q

Gastric phase: control of chief cells (of corpus)- secretin

A

-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
Q

Gastric phase: control of enterochromaffin like cells (ECL) (of corpus)- AcH

A

Bind to M3 receptor➡️stimulate release of HCl

77
Q

Gastric phase: control of ECL (of corpus)- gastrin

A

Help stimulate release of histamine

78
Q

Gastric phase: control of ECL (of corpus)- somatostatin

A

-comes from D cells of corpus, not the antral D cells
-inhibits release of histamine

79
Q

Gastric phase: Control of D cells (of corpus)

A

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
Q

basic motility of stomach

A

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
Q

Contents of chyme

A

-glucose
-protons
-partially digested peptides
-Fatty acid

82
Q

Intestinal phase: stimulatory factors- partially digested proteins

A

-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
Q

Intestinal phase: stimulus from partially digested peptides- parietal cells

A

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
Q

Intestinal phase: partially digested peptides stimulus- chief cells

A

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
Q

Pepsinogen➡️pepsin

A

-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
Q

Intestinal phase: entero-oxyntin

A

⬆️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
Q

Intestinal phase: secretin stumuli

A

Stimulates chief cells to make pepsinogen

88
Q

Intestinal phase: inhibitiontory factor- secretin

A

-secreted by S cells
-S cells release secretin in response to:
⬆️ concentration of protons
⬆️ concentration of fats (FA)

89
Q

Functions of secretin in the stomach

A

-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
Q

Functions of secretin in the liver

A

-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

91
Q

Bile contents

A

-bile acids and salts
-phospholipid
-cholesterol
-pigments
-water
-electrolyte chemicals

92
Q

Functions of secretin in the liver

A

-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

93
Q

Intestinal phase: inhibiory factor- CCk

A

Release by entero-endocrine I cells which is stimulated by high concentration of:
-FA (fatty chyme)
-partially digested proteins
-oligosaccharides (hyperosmolar chyme)

94
Q

Function of CCK in the stomach

A

-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

95
Q

Functions of CCK in the liver

A

-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

96
Q

Functions of CCK in the gallbladder

A

-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

97
Q

How does gallbladder help with concentrating bile?

A

By getting rid of a lot of water and electrolytes

98
Q

Functions of CCK in the pancrea

A

-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

99
Q

Intestinal phase: inhibitory factory- peptide YYa d neurotensin chemicals

A

-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

100
Q

Intestinal phase: inhibitory factor- gastric inhibitory peptide (GIP) chemical

A

-Also known as “glucose-dependent insulinotropic peptide”

-Released by enteroendocrine K-cells which responds to
high concentrations of oligosaccharides/polysaccharides and fats

101
Q

Functions of GIP in the stomach

A

-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

102
Q

Functions of GIP in the pancreas

A

-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

103
Q

Intestinal phase: inhibitory factors- AcH

A

Released by the vagus nerve (cranial nerve X) from the central nervous system

104
Q

Functions of AcH in the pancreas

A

-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

105
Q

Functions of AcH in gallbladder

A

Bind to the receptors in the gallbladder → help in gallbladder contractions

106
Q

Intestinal phase: inhibitory factors- chemoreceptors

A

-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

107
Q

Intestinal phase: chemoreceptors- inhibition of parasympathetic outflow

A

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

108
Q

Intestinal phase: chemoreceptors- stimulation of sympathetic outflow

A

-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

109
Q

Protective mechanism of the stomach

A

-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-

110
Q

Mucus gel layer of mucosal barrier

A

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

111
Q

HCO3- of mucosal barrier

A

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

112
Q

Mucosa subdivisions

A

-epithelium
-lamina propria
-muscularis mucosae

113
Q

Mucosa- epithelium subdivision: tissue type

A

Stratified squamous epithelium in the mouth, oropharynx, laryngopharynx, esophagus, and anus

Simple columnar epithelium in the remainder of the canal

114
Q

Mucosa- lamina propria subdivision tissue type

A

Areolar connective tissue w/ blood vessels

Many lymphoid follicles, especially at tonsils and mucosa-associated lymphoid tissue (MALT)

115
Q

Mucosa- muscularis mucosae subdivision: tissue type

A

Thin layer of smooth muscle

116
Q

Functions of mucosa

A

-secretion of mucus, digestive enzymes, and hormones
-absorption of end products into the 🩸
-protection against infectious disease

117
Q

Submucosa tissue type

A

Areolar and dense irregular connective tissue containing blood vessels, lymphatic vessels, and nerve fibers (sub mucosal nerve plexus)

118
Q

Submucosa functions

A

🩸 vessels absorb and transport nutrients

Elastic fibers help maintain the shape of each organ

119
Q

Muscularis externa subdivision of layers

A

-circular layer- liner layer of smooth muscle
-longitudinal layer- outer layer of smooth muscle

120
Q

Functions of muscularis externa

A

Segmentation and peristalsis of digested food along the tract are regulated by meyenteric nerve plexus

121
Q

Serosa (visceral peritoneum) subdivision of layer

A

-connective tissue: Areolar connective tissue
-epithelium (mesothelium): simple squamous epithelium

122
Q

Serosa function

A

Reduces friction as the digestive system organs slide across one another

A&p2 (28 decks)

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