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Gastrointestinal system Flashcards

(60 cards)

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1
Q

What does the nervous system in the GI tract consist of?

A

Intrinsic (enteric) system

Extrinsic system: sympathetic, parasympathetic

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2
Q

Where is the intrinsic nervous system of the GI tract found?

A

In the wall of the GI tract

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3
Q

2 plexuses of GIT intrinsic nervous system

A

Myenteric (Auerbach’s) plexus = between circular and longitudinal muscle layers, mainly motor

Submucosal (Meissner’s) plexus = within submucosa, mainly sensory

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4
Q

What does the enteric nervous system respond to?

A

Responsible for majority of gut SECRETION and MOTILITY

Respond to gut transmitters:
Cholecystokinin
Substance P
Vasoactive intestinal peptide (VIP)
Somatostatin
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5
Q

Input of enteric nervous system apart from gut transmitters

A

From autonomic (extrinsic) nervous system

Sympathetic: fibres terminate in the submucosal and myenteric plexuses

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6
Q

What does stimulation of the GIT SYMPATHETIC nervous system lead to?

A

Vasoconstriction
Inhibit secretion of glandular tissue
Contraction of sphincters
Inhibit circular muscle of bowel, hence DECREASING MOTILITY

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7
Q

What does stimulation of the GIT PARASYMPATHETIC nervous system lead to?

A

Parasympathetic: fibres terminate in MYENTERIC plexus ONLY

Increase secretion of glandular tissue
Relaxation of sphincters
Stimulate circular muscle of bowel, hence INCREASING motility

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8
Q

Hormones and neurotransmitters regulating GI motility and secretion

A 
Gastrin
Secretin
Cholecystokinin (CCK)
Pancreatic polypeptide
Gastric inhibitory polypeptide (GIP)
Motilin
Enteroglucagons
Neurotensin
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9
Q

Which glands secrete saliva?

A

PAROTID (25%) = watery lacking mucus, Na and Cl- lower than plasma, K+ and bicarb levels higher, high enzyme conc (salivary amylase and IgA), affected by aldosterone

SUBMANDIBULAR (70%) = more viscous (mixed serous and mucosal)

SUBLINGUAL (5%) = contain mucoproteins

(numerous saliva glands present over tongue and palate)

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10
Q

Functions of saliva

A 
Lubrication (mucus) to help with swallowing
Speech
Taste
Antibacterial: lysozyme, IgA
Starch digestion: amylase
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11
Q

2-stage process of saliva formation within salivary glands

A

1) ISOTONIC fluid of similar composition to ECF secreted by ACINAR component of salivary gland
2) Isotonic fluid is modified as it moves along the duct. Na and Cl- removed, K+ and HCO3- added by ATP transport proteins

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12
Q

Why is saliva DILUTE during LOW rates of secretion?

A

Plenty of time for ductal modification

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13
Q

Why is saliva more CONCENTRATED during HIGH rates of secretion?

A

Na, Cl- and HCO3- content increases

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14
Q

What is saliva secretion controlled by?

A

Autonomic nervous system

Reflex stimulated by salivary nuclei in MEDULLA

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15
Q

What is saliva secretion STIMULATED by?

A

Stimulation of mechanoreceptors and chemoreceptors in mouth

Higher centres in CNS i.e. smelling/thinking about food

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16
Q

Parasympathetic impulses stimulate saliva secretion through which cranial nerves?

A

Facial and glossopharyngeal nerves

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17
Q

3 phases of swallowing

A

ORAL = voluntary

PHARYNGEAL = involuntary, superior constrictor raises soft palate (preventing food from entering nasopharynx), initiates peristalsis pushing food through upper oesophageal sphincter (respiration inhibited to prevent food entering resp system)

OESOPHAGEAL = peristalsis continues

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18
Q

Pressure of oesophegeal sphincter

A

15-25mmHg (high) in region 2cm above and 2cm below diaphragm

Note: it’s a physiological sphincter, not anatomical

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19
Q

Factors preventing reflux from stomach into oesophageus

A

Physiological oesophageal SPHINCTER

RIGHT CRUS of diaphragm compresses oesophagus as it passes through oesophageal hiatus

ACUTE ANGLE at which oesophagus enters the stomach acts as a VALVE

Closure of sphincter is under VAGAL control, but hormone GASTRIN causes sphincter to CONTRACT

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20
Q

Which hormones cause the oesophageal sphincter to RELAX?

A

Secretin
CCK
Glucagon

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21
Q

What is the gastric mucosa divided into?

A

Columnar epithelium = secrete protective mucus layer

Gastric glands = intersperse mucosa, contain secretory cells

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22
Q

Types of secretory cells in gastric mucosa

A

MUCUS cells = secret mucus, located at OPENING of gastric glands

PEPTIC (chief) cells = at BASE of gastric glands, secrete PEPSINOGEN

PARIETAL (oxyntic) cells = secrete HCl and INTRINSIC FACTOR

NEUROENDOCRINE cells = secrete peptides regulating GI motility and secretion i.e. GASTRIN

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23
Q

Predominant cell types in various regions of stomach

A

FUNDUS and BODY = PEPTIC and PARIETAL cells

ANTRUM and pylorus = MUCUS and NEUROendocrine

CARDIA = gastric glands composed almost completely of MUCUS cells

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24
Q

How much secretion does the stomach produce per day?

A

~2-3L per day

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25
What does gastric secretion contain?
``` HCl Pepsinogen Mucus Intrinsic factor Salt, water ```
26
pH of stomach acid
pH 1-3
27
Roles of stomach acid
Tissue breakdown Convert pepsinogen to active pepsin Form soluble salts with Ca and iron (to aid their absorption) Immune defence mechanism by killing microorganisms
28
What is gastric acid secreted by?
Parietal cells
29
What happens when parietal cells are activated?
Deep clefts form in the apical membrane These canaliculi allow acid to be secreted into stomach
30
How are the H+ and Cl- ions pumped from the parietal cell?
H+ ions pumped by H+/K+ ATPase (K+ going into cell) Cl- ions pumped by 2 routes: 1) Chloride channel 2) Cl-/K+ co-transport system (K+ going out of cell)
31
How are H+ ions produced in the stomach?
By oxidative processes This also produces a OH- ion
32
What happens to the hydroxyl ion produced by parietal cells?
It results in the formation of HCO3- in a reaction catalysed by carbonic anhydrase It is then exchanged for Cl- on basolateral surface of the cell
33
What can the production of HCO3- by parietal cells be influenced by?
Prostaglandins
34
How is acidity of gastric acid maintained?
By H+/K+ ATPase pump on parietal cells | as part of the process, bicarb ions will be secreted into surrounding vessels
35
What happens to the Na and Cl- ions in parietal cells?
Na+ and Cl- ions are ACTIVELY SECRETED from parietal cells into the canaliculus This sets up a NEGATIVE POTENTIAL across the membrane Hence, Na+ and K+ ions diffuse across into the canaliculus
36
What happens to the bicarbonate ions secreted by parietal cell into surrounding vessels?
Carbonic acid is formed This dissociates into H+ ions, which leave the cell via the H+/K+ antiporter pump Na+ ions are actively absorbed at the same time This leaves H+ and Cl- ions in the canaliculus. These mix and are secreted into the lumen of the oxyntic gland
37
Factors protecting stomach from digestion
ALKALINE MUCUS secreted from cells at neck of gastric glands form a layer (mucosal barrier) over gastric epithelium Tight epithelial junctions prevent acid from reaching deeper tissues Prostaglandin E secretion increases thickness of mucus layer, stimulating HCO3- production and increasing blood flow in mucosa (bringing nutrients to any damaged areas)
38
3 phases of gastric acid secretion
CEPHALIC (smell/taste of food) = 30% of acid produced, VAGAL cholinergic stimulation causing HCl secretion and GASTRIN release from G cells GASTRIC (stomach distension) = 60% of acid produced, stomach distension/low H+/peptides causes GASTRIN release INTESTINAL (food in duodenum) = 10% of acid, high acidity/distension/hypertonic solutions in duodenum INHIBITS gastric acid secretion via enterogastrones (CCK, secretin) and neural reflexes
39
Factors increasing gastric acid production
VAGAL NERVE stimulation GASTRIN release HISTAMINE release (indirectly following gastrin release) from enterochromaffin-like cells
40
How does vagal activity stimulate gastric secretion?
Direct stimulation of gastric glands via ACh release Gastrin release from G cells in atrum (stimulate acid and pepsin secretion, and histamine release) Histamine release from mast cells (stimulates parietal cells via H2 receptors, causing acid production)
41
Factors decreasing gastric acid production
Somatostatin (inhibit histamine release) CCK Secretin
42
Source, stimulus and action of GASTRIN
Source = G cells in antrum of stomach Stimulus = stomach distension, extrinsic nerves (inhibited by low antral pH and somatostatin) Actions = increase HCl, pepsinogen and IF secretion, increase gastric motility, trophic effect on gastric mucosa
43
Source, stimulus and action of CCK
Source = I cells in upper small intestine Stimulus = partially digested proteins and triglycerides (fatty food in duodenum) Actions = increase secretion of enzyme-rich fluid from pancreas, gallbladder contraction, relaxation of sphincter of Oddi, decrease gastric emptying, trophic effect on pancreatic acinar cells, induce SATIETY
44
Source, stimulus and action of SECRETIN
Source = S cells in upper small intestine Stimulus = acidic chyme, fatty acids Actions = increase secretion of bicarb-rich fluid from pancreas and hepatic duct cells, decrease gastric acid secretino, trophic effect on pancreatic acinar cells
45
Source, stimulus and action of VIP
Source = Small intestine, pancreas Stimulus = neural Actions = stimulate secretion by pancreas and intestines, inhibit acid and pepsinogen secretion
46
Source, stimulus and action of SOMATOSTATIN
Source = D cells in pancreatic islets and stomach Stimulus = fat, bile salts, glucose in intestinal lumen Actions = decrease acid, gastrin and pepsin secretion, decrease pancreatic enzyme secretion, decrease insulin and glucagon secretion, inhibit trophic effects of gastrin, stimulate gastric mucus production, inhibit growth hormone
47
What type of saliva does parasympathetic stimulation produce?
Water-rich, serous
48
What type of saliva does sympathetic stimulation produce?
Low volume, enzyme-rich
49
Where is somatostatin produced?
D cells of pancreatic islets Enterochromaffin cells of gut Brain tissue Note: substances inducing insulin release also induce somatostatin production
50
Clinical application of somatostatin
Treat pancreatic fistulae (as it reduces pancreatic exocrine secretions)
51
Clinical manifestations of somatostatinomas
Diabetes mellitus Gallstones Steatorrhoea
52
Resting volume and pressure of stomach
Volume = 50mL Intragastric pressure = 5-6mmHg
53
Factors increasing rate of gastric emptying
Increased gastric volume | Gastrin release
54
Factors decreasing rate of gastric emptying
Hypertonic CHYME Gastric ACID entering duodenum (vagally-mediated delay in gastric emptying + stimulate bicarb release from pancreas to neutralise acid + secretin release --> inhibit antral contractions + increase contractility of pyloric sphincter) FATTY food (CCK and GIP released by small intestines --> increase contractility of pyloric sphincter) PROTEINS (stimulate gastrin release --> increase contractility of pyloric sphincter)
55
Why do individuals who have undergone truncal vagotomy tend to routinely require either a pyloroplasty or gastro-enterostomy?
Neuronal stimulation of the stomach is mediated via the vagus nerve. The parasympathetic nervous system will tend to favor an increase in gastric motility. Patients with truncal vagotomy would need pyloroplasty/gastro-enterostomy as they would otherwise have delayed gastric emptying.
56
Where is the vomiting centre located in the CNS?
Medulla oblongata
57
Locations of vomiting receptors
Labyrinthine receptors of EAR (motion sickness) Over-distension receptors of DUODENUM and STOMACH TRIGGER ZONE of CNS - many drugs (e.g. opiates) act here Touch receptors in THROAT
58
Events occurring during vomiting
Respiration inhibited Larynx closes and soft palate rises Stomach and pyloric sphincter relax and duodenum contracts, propelling intestinal contents into stomach Diaphragm and abdominal wall contract --> intragastric pressure increases Gastro-oesophageal sphincter relaxes and pylorus closes Stomach contents expelled through the mouth
59
Stimulation of vomiting centre in medulla leads to motor impulses passing along which cranial nerves?
CN 5, 7, 9, 10 to the intercostals, abdominal muscles and diaphragm
60
Causes of vomiting
Stimulation of posterior oropharynx Excessive distension of stomach or duodenum Stimulation of labyrinth e.g. motion sickness Severe pain Raised ICP Stimulation of chemoreceptor trigger zone by noxious chemicals Bacterial irritation of upper GI tract

MRCS Physiology (6 decks)

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