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MRCS Physiology > Gastrointestinal system > Flashcards

Gastrointestinal system Flashcards

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
Q

What does gastric secretion contain?

A 
HCl
Pepsinogen
Mucus
Intrinsic factor
Salt, water
26
Q

pH of stomach acid

A

pH 1-3

27
Q

Roles of stomach acid

A

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
Q

What is gastric acid secreted by?

A

Parietal cells

29
Q

What happens when parietal cells are activated?

A

Deep clefts form in the apical membrane

These canaliculi allow acid to be secreted into stomach

30
Q

How are the H+ and Cl- ions pumped from the parietal cell?

A

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
Q

How are H+ ions produced in the stomach?

A

By oxidative processes

This also produces a OH- ion

32
Q

What happens to the hydroxyl ion produced by parietal cells?

A

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
Q

What can the production of HCO3- by parietal cells be influenced by?

A

Prostaglandins

34
Q

How is acidity of gastric acid maintained?

A

By H+/K+ ATPase pump on parietal cells

as part of the process, bicarb ions will be secreted into surrounding vessels

35
Q

What happens to the Na and Cl- ions in parietal cells?

A

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
Q

What happens to the bicarbonate ions secreted by parietal cell into surrounding vessels?

A

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
Q

Factors protecting stomach from digestion

A

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
Q

3 phases of gastric acid secretion

A

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
Q

Factors increasing gastric acid production

A

VAGAL NERVE stimulation
GASTRIN release
HISTAMINE release (indirectly following gastrin release) from enterochromaffin-like cells

40
Q

How does vagal activity stimulate gastric secretion?

A

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
Q

Factors decreasing gastric acid production

A

Somatostatin (inhibit histamine release)
CCK
Secretin

42
Q

Source, stimulus and action of GASTRIN

A

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
Q

Source, stimulus and action of CCK

A

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
Q

Source, stimulus and action of SECRETIN

A

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
Q

Source, stimulus and action of VIP

A

Source = Small intestine, pancreas

Stimulus = neural

Actions = stimulate secretion by pancreas and intestines, inhibit acid and pepsinogen secretion

46
Q

Source, stimulus and action of SOMATOSTATIN

A

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
Q

What type of saliva does parasympathetic stimulation produce?

A

Water-rich, serous

48
Q

What type of saliva does sympathetic stimulation produce?

A

Low volume, enzyme-rich

49
Q

Where is somatostatin produced?

A

D cells of pancreatic islets
Enterochromaffin cells of gut
Brain tissue

Note: substances inducing insulin release also induce somatostatin production

50
Q

Clinical application of somatostatin

A

Treat pancreatic fistulae (as it reduces pancreatic exocrine secretions)

51
Q

Clinical manifestations of somatostatinomas

A

Diabetes mellitus
Gallstones
Steatorrhoea

52
Q

Resting volume and pressure of stomach

A

Volume = 50mL

Intragastric pressure = 5-6mmHg

53
Q

Factors increasing rate of gastric emptying

A

Increased gastric volume

Gastrin release

54
Q

Factors decreasing rate of gastric emptying

A

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
Q

Why do individuals who have undergone truncal vagotomy tend to routinely require either a pyloroplasty or gastro-enterostomy?

A

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
Q

Where is the vomiting centre located in the CNS?

A

Medulla oblongata

57
Q

Locations of vomiting receptors

A

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
Q

Events occurring during vomiting

A

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
Q

Stimulation of vomiting centre in medulla leads to motor impulses passing along which cranial nerves?

A

CN 5, 7, 9, 10

to the intercostals, abdominal muscles and diaphragm

60
Q

Causes of vomiting

A

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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