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GIT physiology > Stomach > Flashcards

Stomach Flashcards

1
Q

What happens when the bolus of food passes into stomach

A

Lower oesophageal sphincter hypercontracts to prevent reflux

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2
Q

What do specialised cells in the stomach do

A

Synthesise and secrete mucous fluid, enzyme precursors, HCl, hormones

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3
Q

What is responsible for gastric motility

A

Abundant SM in the stomach

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4
Q

Name for “food” in the stomach

A

Chyme

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5
Q

What secretes gastric juice

A

Cells of gastric mucosa

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6
Q

HCl (contained in gastric juice)

A

Cleans food

Protein digestion

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7
Q

Pepsinogen

A

Precursor to pepsin

Digests protein

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8
Q

Intrinsic factor

A

Vitamin B12 absorption in the ileum

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9
Q

Mucus

A

Protects gastric mucosa from acidic environment (H+ - pH 1-2)

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10
Q

PARIETAL CELLS

  1. Location
  2. Secretion
A
  1. Body
  2. HCl and intrinsic factor
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11
Q

CHIEF CELLS

  1. Location
  2. Secretion
A
  1. body
  2. Pepsinogen
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12
Q

G CELLS

  1. Location
  2. Secretion
A
  1. Antrum
  2. Gastrin INTO CIRCULATION
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13
Q

MUCOUS CELLS

  1. Location
  2. Secretion
A
  1. Antrum
  2. Mucus and pepsinogen
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14
Q

D CELLS

  1. Location
  2. Secretion
A
  1. Antrum
  2. Somatostatin
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15
Q

Why is gastrin unusual

A

Secretion is not into the lumen but into bloodstream

PARACRINE secretion

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16
Q

4 types of secretion

A
  1. EXOCRINE - outside of body (going to outer space)
  2. ENDOCRINE - with G cells (radio broadcast, signal to whole body but only people tuning in will listen to the message)
  3. PARACRINE - somatostatin (talking to the neighbours -conc of message decreases to the power of 3 as you move out from source - communicates 10 cells width)
  4. AUTOCRINE - acid secretion (singing to yourself)
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17
Q

What are gastric pits similar to

A

salivary gland

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18
Q

What are the pits lined with

A

Parietal cells

Chief cells

G cells

D cells

Mucus neck cells (secrete mucus and bicarbonate)

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19
Q

Where do regional differences exist

  1. Secretions near lower oesophagus/pyloric sphincter
  2. Secretions in rest of stomach
A

in the number of cell types lining a gastric pit

  1. Mucus, HCO3-
  2. Digestive secretions (H+, pepsinogen)
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20
Q

2 functions of HCl

A
  1. Clean food - make it aseptic, but becteria and viruses can still get through
  2. Denature proteins and break protein bonds
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21
Q

How is HCl secreted

A

At apical membrane, H+ is secreted into lumen of stomach via primary active transport

Cl- follows H+ into the lumen

However, at basolateral membrane, HCO3- is moved into interstitial space in exchange for Cl-

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22
Q

If the pH of the cell increases, what happens

A

Encourages the disintegration of carbonic acid to H2O and CO2

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23
Q

Stimulation of H+ secretion by gastric parietal cells

A

PNS stimulation starts at Vagus (Gs)

HISTAMINE is released from enterochromaffin-like cells in gastric mucosa, binds to nearby PARIETAL cells, binds to H2 receptor, Gs protein, cAMP, PKA increases ATPase activity

** ALL 3 involve PKA

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24
Q

What are ulcers

What was first used to treat it

A

Injury to gastric mucosa, with acid going into it

Atropine - muscarinic antagonist

Now omeprazole - directly inhibitd the H+ K+ ATPase pump

  • reduces acid secretion, prevents acidic environment in the stomach, extremely effective against acid reflux
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25
Inhibition of the H+ K+ ATPase pump - SOMATOSTATIN (D cells)
**_Direct pathway_** * inhibits parietal cells, bind to receptor, Gi, reduced cAMP, reduced H+ secretion * Inhibits G cells **_Indirect pathway_** * Inhibits histamine release from ECL cells * Inhibits gastrin release from G cells
26
How is HCl secreted into stomach nerve-wise
Vagus nerve innervation - parietal cells directly (ACh) =\> HCl release
27
Role G cells play in HCl secretion
G cells (Gastrin-Releasing Peptide) release gastrin into circulation in response to proteins in the meal Carried in bloodstream to parietal cells - HCl is then released via this indirect route
28
What does atropine (muscarinic blocking agent) not fully block
HCl secretion
29
CEPHALIC PHASE 1. How much of total HCl secretion does it account for 2. What are the stimuli 3. What sort of reflex is it 4. What are the mechanisms
1. Accounts for 30% total HCl secretion 2. Smell, taste 3. Conditioned reflex - in anticipation of food 4. Direct and indirect mechanisms
30
GASTRIC PHASE 1. How much of total HCl secretion does it account for 2. What are the stimuli 3. Mechanisms
1. Accounts for 60% of total HCl secretion 2. Distension of stomach and presence of AAs and small peptides 3. DISTENSION - direct and indirect vagal stimulation of parietal cells (gastrin): AA AND PEPTIDES - direct effect on G cells (gastrin) \*\* all converge on G cells and act on an endocrine signal
31
Where do majority of stimuli come from
Lumen
32
INTESTINAL PHASE 1. How much of total HCl secretion does it account for 2. What is its major function 3. Stimulus
1. Accounts for 10% of total HCl secretion 2. Major function is to inhibit acid secretion from stomach and protect SI from acid 3. AAs and peptides stimulate G cells to release gastrin - parietal cells - HCl secretion
33
Name the 5 protective factors
1. HCO3- 2. Mucus 3. Prostaglandins - slightly inhibit gastric secretions) 4. Mucosal blood flow 5. Growth factors
34
Name the 7 damaging factors
1. H+ 2. Pepsin - would also digest mucosa 3. NSAIDs e.g. aspirin 4. stress 5. smoking 6. alcohol 7. Helicobacter pylori - ONLY PATHOGEN NECESSARY FOR GASTRIC ULCERS
35
Why must the gastric mucosa be protected
Mammalian cells cannot survive in an acidic environment as they will denature their own proteins
36
Describe mucosal blood flow
quite high - high buffering capacity - high turnover rate of gastric mucosa
37
Helicobacter pylori How does it damage the mucus layer
One of the few pathogens that can live in the human GIT Uses flagella to embed itself into mucus layer, secretes alkaline substances to neutralise acid, creates a little pocket for itself, doing that means it breaks the mucosa layer and creates a passage for acid to go into and attack cells
38
How does the prevalence of H pylori infection differ between developed and developing countries
NB H pylori is essential for ulcers
39
what does 13C-urea produce
alkaline agents
40
Explain this graph
Black line is control Blue (2) is a patient - 13CO2 will rise as urea is being metabolised by enzyme urease (not in our biome) Graph 3 is normal
41
What does the body do to overcome the noxious effect of pepsin
Chief cell secretes pepsinogen, a precursor to pepsin
42
how is pepsinogen activated
By HCl in lumen of stomach
43
Where does the breakdown of proteins to short peptides by pepsin happen
In lumen, away from mucosa
44
+ve feedback loop of pepsin and pepsinogen
So beginning of meal, HCl stimulates pepsinogen to form pepsin, but then pepsin takes over and controls pepsinogen itself Any pepsinogen rapidly becomes pepsin and action of protease in lumen is intrinsically high - no inactive pepsinogen in stomach
45
2 functions of pepsin
1. Breakdown of proteins, IC matrixes and release nutrients so we're not just producing peptides but breaking down the whole organism together 2. PROTECTION - pepsin is noxious on surface of bacteria, viruses, parasites, shave EC matrix by digesting EC protein, disrupt ion balance and homeostasis, break down any living organism getting into the stomach
46
What does the intrinsic factor do
Binds vitamin B12 Protects it from damage it may suffer in the stomach and LI
47
Where does the B12 and intrinsic factor complex eventually get absorbed
In the ileum
48
What is B12 a co-factor in
Formation of RBCs in bone marrow
49
What is pernicious anaemia
Formation of RBCs is not sufficient which could be as a result of a gastric problem with intrinsic factor
50
Name the 3 reflexes that regulate the relaxation of the gastric reservoir
1. Receptive - feed-forward mechanism, mostly distension but also nutrient sensing from gastric wall, triggering of a vagal vagal reflex 2. Adaptive 3. Feedback-relaxation - nutrients in duodenum cause vagal vagal reflex through tension receptors and release of CCK on vagal afferent neurons
51
Relationship between pressure and vol (derived from Law of Laplace)
P = 2T/R R is proportional to the square root of V so T is proportional to P x Square root of V
52
What does tetrodotoxin do
Binds to site on Na+ VG channel
53
What happens to pressure as vol of stomach increases
The increase in pressure is smaller and smaller
54
Effect of TTX and truncal vagotomy on pressure and vol
The cutting of the vagal nerve shows evidence that we need vagus transmission (neural) to generate gastric relaxation reflex
55
Contribution of different triggers to the gastric accommodation reflex in humans
56
Difference in function between body and antrum
BODY - storage ANTRUM - pump
57
Retention of a viscous meal
58
Plasma glucose over time
Insulin drives glucose out of the bloodstream and into adipose tissue, liver and mostly muscle
59
Relationship between gastric retention and how much glucose entered the blood stream
Retaining the food prevents glucose entering the bloodstream High retention, low plasma glucose
60
Regions of the stomach
61
How is digesta moved from the gastric reservoir into the antral pump
1. Tonic contractions - if tension is high, food will move quickly to the antrum 2. Peristaltic waves
62
Poiseuille's equation for blood flow
n is viscosity of blood lamda (upside down Y) is length of blood vessel ALSO BF = difference in P/Resistance =\> R = 8nλ/πr4 (radius of pyloric sphincter changes greatly - major regulator of gastric emptying)
63
3 phases of the function of the gastric pump
1. Phase of propulsion 2. Phase of emptying 3. Phase of retropulsion
64
Phase of propulsion
Contraction of proximal antrum Propulsion of chyme into relaxing terminal antrum and duodenal contraction pyloric sphincter - diameter 1mm 2-3 of these contractions per min after a meal
65
Phase of emptying
Contraction of middle antrum transpyloric and retrograde flow Duodenal relaxation
66
Phase of retropulsion
Contraction of terminal antrum Jet-like back-flow with grinding Duodenal contraction
67
Sieving function
Lipids and small particles leave the stomach more rapidly than large particles
68
How do we grind solid particles
Forceful jet-like retropulsion through the small orifice of the terminal antral contraction
69
Antro-duodenal co-ordination
Proximal duodenum is silenced when the pyloric sphincter is open When stomach is emptying, duodenum is relaxed and accepting this chyme
70
Balance between gastric reservoir and antral pump What do the 2 reflexes ensure
regulation of rate of delivery of food from body to pump
71
What is pyloric activity modulated by
Antral inhibitory and duodenal excitatory reflexes
72
What is an additional function of the pyloric sphincter
Prevent duodeno-gastric reflux
73
Factors that influence the rate of flow
Viscosity Nutrient density - if energy content of meal is higher it will empty more slowly high osmolality of chyme will delay gastric emptying acidity delays gastric emptying
74
Rate of flow of pyloric sphincter is proportional to Which part of the duodenum has low pressure
Pressure diff (stomach - duodenum) divided by R (diameter of pyloric sphincter) duodenal bulb has low P
75
What happens when oleic acid and bile is added
Pyloric sphincter not only contracts and stays contracted for the whole period after the fat is added, it is HYPERCONTRACTED =\> presence of fat closes pyloric sphincter more strongly than when it was closed before - stays closed for a couple of mins
76
What do the duodenal bulbs do
Show brief spikes - peristatic waves - strong segmentation contractions 1. Reduces drive of pressure in the stomach 2. Increases the pressure in the duodenum 3. Increases R
77
Macronutrients that are best at regulating motility
Fat \> protein \> CHOs \> osmotic load (signals within lumen of GIT)
78
Factors of gastric and duodenal motility that co-operate and modulate gastric emptying
79
How are solids and liquids of the gastric chyme emptied with different velocities
Emptying of liquids is exponential Emptying of large solid particles only begins after sufficient grinding (lag phase) Viscous chyme is then mainly emptied in a linear fashion
80
Differences between a non-caloric and caloric meal
81
Mediation of mechanisms that allow gastric emptying
Nutrients - LCFAs, Aas, peptides from lumen of duodenum stimulating 2 types of receptors Neuronal cells that signal to afferent vagal neurons Stimulate afferent CCK secreting cells that stimulate afferent vagal neurons going to vagal centre and 3 different outputs come out Gastric accommodation reflex - mainly NO Stimulating cholinergic vagal fibres that increase stimulation to pyloric sphincter and ACh release onto antrum to reduce contraction of antrum White arrow - internal reflex contracting pyloric sphincter without needing vagal afferents
82
What impact would a high fat breakfast have on lunch
Lunch would be emptied more slowly Not just responding to the content of the meal, but also the meal preceding it

GIT physiology (11 decks)

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