18-01-23 - Overview of Gastrointestinal Physiology Flashcards

1
Q

Learning outcomes

A
  • Recall the basic structure of the Gastrointestinal Tract
  • Recall the innervation of the Gastrointestinal Tract
  • Compare and contrast the organisation and roles of the extrinsic and intrinsic (enteric) nervous system
  • Describe the different types of Gastrointestinal tract motility and their functions
  • Describe the electrophysiological properties of Gastrointestinal Tract smooth muscle cells
  • Describe the neural and endocrine regulation of Gastrointestinal Tract motility
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2
Q

What 8 things does the GI tract consist of?

What is an additional component of this?

How is the gut separated into sections?

A
  • 8 things the GI tract consists of:
    1) Mouth
    2) Oesophagus
    3) Stomach
    4) Small intestine
    5) Large intestine
    6) Appendix
    7) Rectum
    8) Anus
  • In addition to this, there are accessory organs
  • The gut is separated into ‘sections’ by Sphincters
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3
Q

What are 4 stages in the overview of food moving through the GI tract?

A
  • 4 stages in the overview of food moving through the GI tract:

1) Ingestion of food
* Mastication
* Swallowing

2) Motor functions of the stomach
* Storage
* Mixing/propulsion of food
* Stomach emptying & its regulation

3) Movements of the small intestine
* Mixing contractions
* Propulsive movements
* Prevention of backflow

4) Movements of the large intestine
* Mixing/propulsive movements
* Defecation

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4
Q

What does the surface of the GIT have to be equipped to deal with?

Why are their different layers in the GIT?

Label the layers of the GIT.

Name the 9 layers of the general structure of the GIT from the lumen to the outside of the tube

A
  • The GIT is always exposed to the external environment, so must be equipped to deal with this
  • The GIT has many different layers, that each have a different function.
  • 9 layers of the general structure of the GIT from the lumen to the outside of the tube:
    1) Epithelium,
    2) Lamina propria
    3) Muscularis mucosa
    4) Submucosa
    5) Submucosal plexus
    6) Circular muscle
    7) Myenteric plexus
    8) Longitudinal muscle
    9) Serosa
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5
Q

What are the layers from top to the bottom in the microanatomy of the GIT?

What does each layer consist of?

A
  • Layers from top to the bottom in the microanatomy of the GIT:
  • The outer most layer of the GIT is the mucosa, which consists of epithelium, lamina propria (connective tissue), and the muscularis mucosa
  • The submucosa layer consists of blood vessels and nerve bundles that form the submucosal plexus (Meissner plexus), which is an integral part of the enteric nervous system.
  • The muscularis externa consists of 2 smooth muscle layers – circular muscle and longitudinal muscle. Between these 2 layers lies the myenteric (Auerbach) plexus)
  • The serosa (adventitia) is the bottom layer, and consists of connective tissue and squamous epithelial cells
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6
Q

What parts of the general organisation of the GIT wall are missing at different segments?

What structure is found predominantly in small and large intestine?

What structure is present throughout all of the GIT?

A
  • All parts of the GIT except the oesophagus and the distal rectum have the general organisation of the GIT shown on the previous cards
  • The oesophagus and the distal rectum lack the serosa (adventitia) and mesentery
  • Submucosal plexus is found predominantly in small and large intestine
  • Myenteric plexus present throughout GIT, as it sits on top of the longitudinal muscle, so it is necessary throughout all of the GIT
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7
Q

Splanchnic circulation.

Where does the liver receive venous blood from?

Where does venous blood go after the liver?

What is the purpose of this process?

A
  • Splanchnic circulation
  • Blood from gut, spleen & pancreas flows to the liver via portal vein
  • After venous blood is filtered by liver sinuses, it leaves via the hepatic veins into the vena cava
  • The purpose of this process is to Allow for the removal of bacteria/particulate matter (by recticuloendothelial cells) that might enter the blood from the GI tract
  • This prevents direct transport of potentially harmful agents into body
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8
Q

What are the 3 major arteries that feed the GI system?

What areas are each responsible for supplying?

What 3 other structures do these arteries go onto supply?

What 4 ways is blood flow regulated in the GI tract?

A
  • 3 major arteries that feed the GI system:

1) Celiac trunk – liver, pancreas, stomach

2) Superior mesenteric artery – smallest intestine and most of large intestine

3) Inferior mesenteric – terminal portions of large intestine and rectum

  • Arteries branch and send smaller arteries circling in both directions around the gut
  • Circling arteries branch to smaller arteries penetrate the intestinal wall and spread:
    1) Along the muscle bundles
    2) Into the intestinal villi
    3) Into submucosal vessels beneath the epithelium
  • 4 ways blood flow in the GIT is regulated:

1) The autonomous nervous system
* Parasympathetic (vasodilator)
* Sympathetic (vasoconstrictor)
* Enteric (vasodilator)

2) Hormonal (endocrine) control
* Adrenaline (epinephrine) – vasoconstriction and vasodilation
* Gastrin (vasodilator)

3) Local (paracrine) control
4) Low Po2 (vasodilator)

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9
Q

Describe the microvasculature of a villus (pleural - villi).

What is this system called?

What is the purpose of this system?

How is villus blood flow controlled?

What is blood flow in the GIT related to?

What 4 things can cause an increase in blood flow in the GIT?

How can GIT disease affect villi?

A
  • The microvasculature in a villus consists of small arterioles and venules that interconnect with a system of multiple looping capillaries
  • This system is called a countercurrent system and provides the best capacity for absorbing nutrients from the gut
  • Villus blood flow is controlled by the highly muscular and highly active walls of the arterioles
  • In the GIT, blood flow is directly related to level of local activity
  • 4 things that can cause an increase in blood flow in the GIT:

1) Vasodilators released from GI mucosa (CCK - cholecystokinin, VIP - vasoactive intestinal peptide, gastrin, secretin) –

2) Vasodilators released from GI glands (bradykinin)

3) Decreased O2 concentration in gut wall due to increased metabolism –

4) Subsequent adenosine release

  • During GIT disease, villi can be disrupted/blunted by lack of oxygen
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10
Q

What part of the GIT is affected by parasympathetic stimulation?

What changes does parasympathetic stimulation bring in the GIT?

What change does sympathetic stimulation bring about in the GIT?

When will this occur?

A
  • Parasympathetic stimulation affects the stomach and lower colon
  • Parasympathetic stimulation leads to increases in blood flow (vasodilation) and glandular secretion
  • Sympathetic stimulation in the GIT leads to vasoconstriction of arterioles
  • This will occur during exercise
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11
Q

What is the enteric nervous system?

What does it control?

Where does it receive input from?

What 2 systems make up the enteric nervous system?

What are the extrinsic (sympathetic and parasympathetic) controls of GIT function?

What excites and inhibits this system?

What are the 3 intrinsic (enteric) controls of GIT function?

What do GIT motilities not require?

What are GI motilities generated by?

What factors only modify but don’t generate GIT motilities?

What 4 factors does the enteric nervous system regulate?

A
  • The enteric nervous system or intrinsic nervous system is one of the main divisions of the autonomic nervous system
  • It controls the function of the gastrointestinal tract
  • The enteric nervous system receives input from the ANS, but can function independently from it
  • The enteric nervous system is made up of the myenteric plexus and the submucosal plexus
  • Extrinsic (sympathetic and parasympathetic) control of GIT function is neural and hormonal
  • Acetylcholine excites this system, while Noradrenaline / adrenaline inhibits
  • Intrinsic (enteric) control of GIT function is myogenic, neural and chemical
  • All GIT motilities do not require external nerve supply
  • GIT motilities are generated by the enteric nervous system
  • Extrinsic factors can’t generate GIT motilities, only modify them
  • 4 factors the enteric nervous system regulates:
    1) Smooth muscle
    2) Secretory cells
    3) Endocrine cells
    4) Blood vessels
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12
Q

How many neurons are in the enteric nervous system?

What does it consist of?

What does it receive input from?

Where does the myenteric and submucosal plexuses lie?

What do they each control?

What 3 things does the submucosal plexus innervate?

A
  • There are approximately 100 million neurons in the enteric nervous system (same as spinal cord)
  • The enteric nervous system consists of sensory, inter, and motor neurons
  • It receives input from the ANS, but can
    function independently from it
  • The myenteric plexus lies between circular and longitudinal smooth muscle layers and innervates both muscle layers
  • The myenteric plexus is mainly concerned with motor control of the GIT
  • The submucosal plexus lies between the circular smooth muscle layer and the mucosa
  • The submucosal plexus controls GIT secretion & local blood flow
  • 3 things the submucosal plexus innervates:

1) Glandular epithelium

2) Endocrine glands

3) Blood vessels

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13
Q

What makes up the extrinsic nervous system?

What are 3 sources of parasympathetic neurons in the extrinsic nervous system?

What do parasympathetics in the extrinsic nervous system innervate?

What is the main function of this?

What are 3 origins of sympathetic neurons in the extrinsic nervous system?

What 3 places do sympathetic nerves terminate in the enteric nervous system?

What is the main function of this sympathetic innervation?

A
  • The extrinsic nervous system is made up of sympathetic and parasympathetic branches of the autonomic nervous system
  • 3 sources of parasympathetic neurons in the extrinsic nervous system:
    1) Branches of vagus nerve
    2) Branches of pelvic nerve
    3) Branches of splanchnic nerve

 Parasympathetics in the extrinsic nervous system innervate neurones in the myenteric plexus
* The main function is to stimulate GIT motility and secretion

  • 3 origins of sympathetic neurons in the extrinsic nervous system:
    1) Celiac plexus
    2) Superior and inferior mesenteric plexuses
    3) Hypogastric plexus

 The sympathetic nerves of the enteric nervous system terminate on the:
1) Enteric nerves
2) The smooth muscles
3) The mucosa

 The main function of this innervation is to inhibit GIT motility and secretion

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14
Q

How large are smooth muscle cells?

How are they organised?

Do they have striations?

How many nuclei do they have?

Are they under voluntary or involuntary control?

What 3 things can they be controlled by?

How is smooth muscle organised in the intestinal tract?

A
  • Smooth muscle cells are small – about 100-200µm in length
  • They are spindle shaped cells arranged in sheets that are perpendicular to each other, and are less regularly organised
  • Smooth muscle cells do not have striations
  • They have a single nucleus
  • They are under involuntary control
  • Smooth muscle cells can be controlled by:
    1) Autonomic Nervous System
    2) Hormones
    3) Stretch
  • Smooth muscle in the intestinal tract is arranged in longitudinal and circular layers
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15
Q

What are dense bodies?

What is their role?

How are smooth muscle cells electrically connected?

How are smooth muscle cells structurally connected?

How does contraction rate of smooth muscles compare with that of skeletal and cardiac muscles?

What control are smooth muscles under?

What occurs when smooth muscle contracts?

What does this allow?

What is this due to in the intestines?

What is the role of dense plaques?

A
  • Dense bodies are non-contractile, but tether actin and myosin within the cell, and transmit mechanical forces within its tissues
  • Smooth muscle cells are electrically connected via gap junctions, so a wave of excitation can be passed from one muscle cell to another (impulse conduction)
  • Smooth muscle cells are structurally connected by focal adhesions, which transmit forces so the smooth muscle can contract in unison
  • Contraction rate of smooth muscle is slow, but also longer than that of cardiac or smooth muscle
  • Smooth muscles are under control from the Autonomic Nervous System (ANS)
  • When smooth muscle undergoes contraction, it shortens longitudinally like skeletal muscles, but is also squeezed sideways
  • This allow something to be pushed through in an organised manner, which is down to the organisation of the longitudinal and transverse circular muscles around the intestines
  • Dense plaques allow for contractile arrays to be anchored to the sarcolemma
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16
Q

How is GI smooth muscle stimulated?

What cells initiate this?

What are the 2 types of electrical activity in the GI smooth muscle?

How does the resting membrane potential differ throughout the GIT?

A
  • GI smooth muscle is stimulated by continual slow, intrinsic electrical activity
  • Interstitial Cells of Cajal (ICC) in the stomach initiate this electrical activity
  • 2 types of electrical activity in the GI smooth muscle:

1) Slow waves
* Continual increasing and decreasing electrical activity
* Basal electrical rhythm (BER); pacesetter potentials

2) Spike potentials
* If there is an increase in electrical activity, then action potentials (spike potentials) can be superimposed on the slow waves, which will lead to the contraction of smooth muscle

  • The resting membrane potential can differ throughout the GIT
17
Q

Are slow waves action potentials?

Do they initiate smooth muscle contraction?

How do they contribute to contraction of smooth muscle?

What are intensity and frequency ranges of slow waves?

A
  • Slow waves are not action potentials but slow undulating changes in resting membrane potential
  • Slow waves do not themselves cause muscle contraction
  • If there is an increase in electrical activity, then action potentials (spike potentials) can be superimposed on the slow waves, which will lead to the contraction of smooth muscle
  • The intensity of slow waves varies between 5 and 15mV
  • The frequency of slow waves ranges from 3-12 per minute
18
Q

What are spike potentials?

When will spike potentials occur?

How does slow wave potential affect the frequency of spike potentials?

How long do spike potentials last?

What 2 things can vary baseline membrane potential?

What 3 things is depolarisation stimulated by?

What 2 things is hyperpolarisation stimulated by?

A
  • Spike potentials are true action potentials
  • If the resting membrane potential reaches >-40mV, then action potentials (spike potentials) will occur automatically on top of slow waves, which will lead to the contraction of smooth muscle
  • The higher the slow wave potential, the greater the frequency of spike potentials
  • Spike potentials each last 10 to 20ms
  • 2 things can vary baseline membrane potential:
    1) Depolarisation leads to increased excitability
    2) Hyperpolarisation leads to decreased excitability
  • 3 things depolarisation is stimulated by:
    1) Stretch
    2) Acetylcholine
    3) Parasympathetics (contraction of GIT as part of rest and digest)
  • 2 things hyperpolarisation isstimulated by:
    1) Norepinephrine
    2) Sympathetics (fight or flight moves blood away from GIT)
19
Q

What voltage does the membrane potential of smooth muscle cells fluctuate between?

Where is electrical activity in the GIT initiated from?

How is this done?

How is it terminated?

A
  • The membrane potential of smooth muscle cells fluctuates between -65 and -45mV
  • Electrical activity in the GIT is Initiated in pacemaker cells known as interstitial cells of Cajal (ICC)
  • This is mainly due to the opening of calcium ion channels leading to the influx of Ca2+ into the cells.
  • Electrical activity is terminated by Ca-dependent K+ efflux.
20
Q

What are 2 main types of GI motility?

A
  • 2 main types of GI motility:

1) Fed state
* Peristalsis and mixing movements

2) Interdigestive state (between meals)
* Also known as the migrating motor complexes (MMCs)

21
Q

What is peristalsis?

What causes peristalsis?

When and where does it occur?

What direction does peristalsis move in?

When might it be reversed?

What is needed for peristalsis to occur?

Describe the process of peristalsis

A
  • Peristalsis is the involuntary constriction and relaxation of the muscles of the intestine or another canal, creating wave-like movements that push the contents of the canal forward.
  • Peristalsis is caused by an automatic reflex (peristaltic reflex) in response to stretch of the GIT wall
  • Peristalsis occurs during fed state in all parts of the GIT from the oesophagus to rectum
  • Peristalsis always moves in an oral to rectal direction at 2 to 25 cm/s
  • Under pathological conditions, peristalsis can be reversed leading to conditions such as vomiting
  • An active myenteric plexus is needed for peristalsis to occur
  • Process of peristalsis - The stretch initiates the circular muscles behind (oral) a bolus to contract (ascending excitatory reflex) and the circular muscles in front (anal) of it to relax (descending inhibitory reflex)
22
Q

Describe the process of neurons being stimulated in peristalsis

A
  • Process of neurons being stimulated in peristalsis:
  • A bolus in the GIT stimulates sensory neurones
  • The sensory neurones activate ascending excitatory cholinergic neurones (release either Ach or substance P), which results in smooth muscle contraction
  • Sensory neurones also stimulate descending inhibitory cholinergic neurones
  • Synapsed to inhibitory motor neurones that release NO/VIP (nitric oxide / vasoactive intestinal peptide), which results in smooth muscle relaxation
23
Q

What is the function of segmentation?

What does segmentation involve?

Describe the process of segmentation

A
  • The function of segmentation it to mix digested food
  • Segmentation involves contractions of circular muscle layer at short intervals along GIT
  • For segmentation to begin, contractions start as in 1 (on diagram)
  • Contractions then move forward to now contract in original relaxed area (2 opposite)
24
Q

When do migrating motor complexes (MMCs) occur?

What is the function of MMC?

What are the 4 phases of MMCs?

How long do they each last?

A
  • Migrating motor complexes (MMCs) occur during periods of fasting / between meals
  • The function of MMC is to clear the stomach and small intestine of debris and bacteria
  • 4 phases of MMCs:

1) Phase I (45-60 mins)
* Quiescent period with slow waves

2) Phase II (30-35 mins)
* Action potential activity on slow waves but sporadic contractions of circular muscle

3) Phase III (2-12 mins)
* Action potential activity on slow waves but regular contractions of circular muscle

4) Phase IV
* Period in which action potential activity and contraction reduce and merge into phase I

25
Q

Endocrine Control of Gastrointestinal Tract Motility

A