2. Stomach Flashcards

1
Q

What are the three phases of Digestion?

A

Cephalic
Gastric
Intestinal!

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2
Q

Desribe the Cephalic Phase

A

This phase occurs before food enters the stomach and involves the preparation of the body for eating and digestion. Sight and thought stimulate the cerebral cortex. Taste and smell stimulus is sent to the hypothalamus and medulla oblongata. After this it is routed through the vagus nerve and release of acetylcholine. Gastric secretion at this phase rises to 40% of maximum rate. Acidity in the stomach is not buffered by food at this point and thus acts to inhibit parietal (secretes acid) and G cell (secretes gastrin) activity via D cell secretion of somatostatin.

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3
Q

Describe the Gastric Phase

A

this phase takes 3-4 hours. It is stimulated by the distension of the stomach, presence of food in stomach and decrease in pH. Distension activates long and myenteric reflexes. This activates the release of acetylcholine, which stimulates the release of more gastric juices. As protein enters the stomach, it binds to hydrogen ions, which raises the pH of the stomach. Inhibition of gastrin and gastric acid secretion is lifted. This triggers G cells to release gastrin, which in turn stimulates parietal cells to secrete gastric acid. Gastric acid is about 0.5% hydrochloric acid (HCl) which lowers the pH to the desired pH of 1-3. Acid release is also triggered by acetylcholine and histamine.

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4
Q

Intestinal Phase

A

Intestinal Phase- this phase has 2 parts, the excitatory and inhibitory. Partially digested food fills the duodenum. This triggers intestinal gastrin to be released. Enterogastric reflex inhibits vagal nuclei, activating sympathetic fibers causing the pyloric sphincter to tighten to prevent more food from entering, and inhibits local reflexes.

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5
Q

CEPHALIC PHASE*

Describe the preparation of GIT for food!

A

Preparing GIT for food:
• Triggers (smell, taste, thought of food)
• Parasympathetic outflow (CNX); Ach
Salivation
Increases stomach secretion: mucous, chief, parietal, G cells
Stimulates pancreatic secretion (Readiness)
• 30% of stomach secretions
• 25% of pancreatic secretions

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6
Q

How does Salivation occur?

A

Salivation
• Both conditioned and simple reflexes
• Sensory: cranial nerves
o Touch: Trigeminal (CNV)
o Taste: Facial (CNVII), glossopharyngeal (IX), vagus (X)
• Integrated by salivatory nuclei in the brainstem
• Visceral motor nerves (PSNS via CNs)
o Submandibular, sublingual: facial (VII)
o Parotid: glossopharyngeal (IX)

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7
Q

Describe Deglutition

A

Neural control only
Voluntary initiation, then pattern generator:
• Food in pharynx initiates swallowing reflex
• Pharyngeal constrictor muscles
• First third of the oesophagus
Continues via ENS
• Lower third of oesophagus
• Peristaltic waves
• Upper/lower oesophageal sphincters (UES/LES) coordinate.

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8
Q

Describe the swallowing Reflex

A

• Counscious or (more often) reflex pharynx stimulation
• Around 1000 times a day, including sleep
• Sensory: tactile receptors in entry to pharynx
• Activates swallowing center in medulla & lower pons
• Motor:
o Cranial nerves to pharynx and upper oesophagus
o Vagus to rest of oesophagus
o “Pauses” pontine respiratory center

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9
Q

Describe the Oropharyngeal Sequence

A
  1. Soft Palate Elevates, closes entry to nose
  2. Vocal cords close, larynx elevates
  3. Epiglottis closes
  4. Pause in breathing
  5. Briefly relax UES (reflex opening after food passes)
  6. Contract upper oesophagus (skeletal muscle)
  7. Initiation of peristaltic wave
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10
Q

Describe the Oesophageal Sequence

A

• Primary peristaltic wave moves at 3-4cm/s for 6-8s
• If bolus is not cleared, oesophageal distension triggers a secondary peristaltic wave (ENS reflex)
• Upper third is skeletal muscle (longitudinal/circular); lower third is smooth muscle, with a gradient in between
• Skeletal and smooth muscles innervated by vagal efferents
o Neuromuscular junctions on skeletal muscle
o Control ENS motor neurons in smooth muscle part.

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11
Q

How does vomitting occur?

A
•	Usually short-lived / adaptive
•	Often preceded by nausea
•	Medullary trigger zone
•	SNS, PSNS activity
o	Sweating, pallor
o	Tachycardia, tachypnea
o	Salivation (protect teeth)
o	Increased gastric tone
•	Deep inspiration against closed glottis (decreased thoracic pressure, increase abdominal pressure)
•	Contract abs, relax LES/ UES
•	Close nasopharynx with soft palate! (danger of aspiration)
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12
Q

GASTRIC PHASE*

A

Digestion of food in the stomach
Stimulated by distension, increased pH, proteins, peptides
Vagus/ENS: stimulates parietal and chief cells (ACh); G cells (GRP); increases motility (mixing waves)
Hormonal: peptides and AAs in the antrum detected → G cells → Gastrin → parietal/chief cell secretion + increases motility
Paracrine: distension + vagus stimulate ECL cells → histamine → parietal acid production
60% of stomach secretions
5-10% of pancreatic (weak gastrin, vagal stimulus)

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13
Q

Describe the stomach secretions
- Into Lumen
Onto Mucosal surface
0Into Blood

A
Into lumen
o	Acid 
o	Pepsinogen
o	Intrinsic Factor
Onto mucosal surface
o	Mucous
o	Bicarbonate- resist breakdown
Into blood
o	Gastrin
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14
Q

Describe the cells present in Gastric Pits

A
Parietal (oxyntic) cells
o	Secrete HCl and intrinsic factor
o	Composition changes with flow rate:
      ---> Na+, K+, Cl- (low) to H+, Cl- (high)
Chief (peptic) cells
o	Secrete pepsinogen
Mucous cells
•		Secrete protective mucous
Glycoprotein layer
Resists pepsin and acid
G (endocrine) cells
o	Secrete gastrin
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15
Q

What is Intrinsic Factor? What does it do?

A
  • Secreted by parietal cells along with acid
  • Forms a dimer complex (blue) with vitamin B12
  • Resistant to pepsin digestion
  • IF-B12 complex binds to a specific receptor (green) in the ileum, internalized
  • B12 is needed for erythrocyte production: IF deficiency -> pernicious anemia.
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16
Q

Acid Secretion

A

Resting: fluid is like ECF
Activated parietal cells:
• Acid from CO2 via Carbonic Anhydrase (CA)
• Proton pump: H+ out, K+ in
• Cl- into lumen (electrogenic; balanced by K+ leak channels)
• HCO3- dumped into blood in exchange for Cl-
Proton pump is drug target
“Alkaline tide” Caused in blood; important in acid overproduction or vomiting

17
Q

Explain Pepsin Secretion

A

Chief (peptic) cells; pepsinogen (pepsin + blocking peptide)
Peptide bond is pH sensitive (breaks if pH <5.5)
Pepsin is then autocatalytic
Digests 10-20% of ingested protein
Stimulated by input from the nerve plexuses, and by acid lumen
Factors affecting acid affect pepsin (gastrin, Ach, secretin, somatostatin, GIP)
Pepsin degradation of muscosal cells is significant in PUD damage

18
Q

What are the VAGUS Stomach secretagogues?

A

Excitatory actions activate proton pumps in membrane
Vagus
o ACh → M3 on parietal cells → Acid
o GRP → GRPR on G cells → Gastrin

19
Q

What are the ENDOCRINE Stomach secretagogues?

A

Endocrine
o Gastrin secreted by G cells in the antrum of the stomach
o Competitor/inhibitors: CCK, secretin, GIP, somatostatin
—> Somatostatin elicited by acid effects on D (short for “D”) cells

20
Q

What are the PARACRINE Stomach secretagogues?

A

Paracrine
o Vagal ACh → M3 on ECL (enterochromaffin-like) cells → histamine
o Histamine → parietal cell H2 receptor

21
Q

Describe the three major secretagogues that interact during all phases of gastric secretion.

A

During the cephalic phase of secretion, acetylcholine and gastrin are released by neuroendocrine mechanisms. In the gastric phase, other stimuli activate acetylcholine and gastrin release. Histamine is released in all phases of secretion.

22
Q

Describe the pathway of secretion

A
  1. Food or cephalic reflexes initiate gastric secretion
    - - vagus nerve &OR Amino Acid + peptides.. –> stimulate G cell –> gastrin secretion
  2. Gastrin stimulates acid secretion
    - -Histamine
  3. Acid stimulates a short reflex secretion of pepsinogen (via chief cells)
  4. Somatostatin is the negative feedback signal.
23
Q

What is mucous stimulated by?

A

• Paracrine
o Vagal ACh → M3 on ECL (enterochromaffin-like) cells → histamine
o Histamine → parietal cell H2 receptor

*pepsin breaks down mucous.
Normal stomach lumen with gastric juice has a pH of -2.
pH -7 at cell surface.
HC03- (bicarbonate) is the chemical barrier that neutralises the acid

24
Q

Muscarinic receptors

A

• M3 may be most relevant
o Smooth muscle contraction
o Parietal cell acid secretion
o ECL stimulation -> histamine -> parietal H2

25
Q

Describe Gastric motility.

A

Highly compliant upper part (cardia, fundus, body)
Peristaltic lower part (antrum, pylorus)
Contraction intensifies towards pylorus
Pyloric sphincter allows small chime releases
Remainder undergoes retropulsion- mixing

26
Q

What is the Basal Electric Rhythm?

A

• -3 per min in stomach, 12 per min in duodenum
• BER differs from other pacemakers (eg. Cardiac)
o Lower frequency (max -40/min, typically 3-12/min)
o Lower amplitude (do not overshoot over 0mV)
o Longer duration (many seconds)

27
Q

How is the BER generated?

A
  • ICC’s are concentrated between the two muscle layers in “pacemaker” regions
  • Connected by gap junctions to muscle layers and other ICCs → spreading depolarization
  • Tight synapses with ENS motor neurons
  • Different GI sections have separate rhythms governed by separate ICC clusters
28
Q

Desribe the Electrical Activity of the Stomach

A

Slow BER waves spread from pacemaker zone in the middle corpus
Size of BER increases towards antrum
In antrum, BER amplitude exceeds threshold for AP
AP resembles a cardiac AP, but it 10x longer

29
Q

Describe Contractile Activity in the stomach

A
Contraction threshold <AP threshold
Strength of contraction increases with 
•	Amplitude of slow wave
•	Time above threshold
Contraction is much stronger if slow wave triggers Aps
Slow wave amplitude and plateau duration
•	Increased by ACh and gastrin
•	Decreased by NE (sympathetics decrease digestion)
30
Q

Describe Gastric Emptying and food composition

A

• SI digests different nutrients at different rates
• Thus reflexes regulate gastric emptying rate depending on food composition
• IF alcohol is consumed with fatty food, lipids slow gastric emptying which keeps alcohol in stomach longer
• EtOH absorption there is slower than in duodenum
o Time bomb effect