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Unit 10 > Week 1: GI motility > Flashcards

Week 1: GI motility Flashcards

1
Q

What is the key descriptor of motility in the GIT?

A

Is controlled

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2
Q

What processes does motility int he GIT influence?

A

Swallowing
Gastric mechanical digestion
Gastric emptying
Intestinal absorption of nutrients and water
Defecation

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3
Q

What is the serosa surface of the GIT?

A

The surface facing the blood (opposed to the lumen)

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4
Q

What is the main component of the lamina propria?

A

Connective tissue
Blood and lymph vessels

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5
Q

What is the main component of the muscularis mucosae?

A

Smooth muscle cells

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6
Q

What is the main component of the submucosal layer?

A

Collagen
Elastin
Glands
Blood vessels of the GIT

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7
Q

What provides motility to the GIT?

A

Two layers of smooth muscle found in the muscularis externa
Inner circular and outer longitudinal muscle

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8
Q

What is the difference between the longitudinal and circular muscle found in the muscularis externa in the GIT?

A

Longitudinal - outermost layer, thin and contains few nerve fibres
Circular - thick and more densely innervated

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9
Q

What are the two different sheets of innervation in the GIT?
Where are they found?

A

Sub-mucosal plexus or mesenteric plexus - in the submucoa
The myenteric plexus - between the circular and longitudinal smooth muscle layers in the muscularis externa

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10
Q

What are the features of smooth muscle?

A

Non-striated : no orderly arranged sarcomeres
Actin and mysoin make up the thin and thick filaments
intermediate filaments such as desmin and dense bodies act as anchor points for contractile filaments and may modulate contractile activity

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11
Q

What is smooth muscle specialised for?

A

Long term and maintained contraction using limited amounts of ATP

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12
Q

What is the ratio of thin to thick filaments in smooth muscle and how does this compare to skeletal muscle?

A

Smooth betwee 12:1 to 18;1 thin to thick
in skeletal muscle 2:1 thin to thick ration

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13
Q

What are dense bodies in smooth muscle?

A

Anchoring sites for actin filaments in smooth muscle

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14
Q

What molecule does skeletal muscle contain in much larger amounts than smooth muscle?

A

Troponin

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15
Q

What is the basic mechanism of Ca2+ dependent smooth muscle contraction?

A
  1. Calcium ion influx into cell increases IC conc.
  2. Ca2+ binds reversibly to calmodulin forming a calmodulin-calcium complex (CaM)
  3. This binds to and activates myosin light chain kinase (MLCK)
  4. This phosphorylates one light chain in each myosin head
  5. The head can now bind repetitively with actin filament and cause muscle contraction (and ATP consumption)
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16
Q

What happens in smooth muscle when Ca2+ ions decrease leading to relaxation?

A

The MLCK become inactive
Myosin light chain phosphatase (MLCP) dominates.
Myosin P is dephosphorylated resulting in muscle relaxation

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17
Q

What are the two different methods by which calcium ions can enter the smooth muscle cell cytoplasm?

A

Pharmacomechanical coupling
Electromechanical coupling

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18
Q

What is electromechanical coupling as a method of calcium transport in smooth muscle cells?

A

Changes in surface membrane potential (typically membrane depolarisation) results in the opening of voltage gated Ca2+ channels causing a rise in intracellular Ca2+ in the cytoplasm

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19
Q

What is pharamacomechanical coupling as a concept in calcium ion movement in smooth muscle cells?

A

Channels respond to chemical and intracellular secondary messengers to cause calcium ion influx into the cytoplasm from the SR and by-non-voltage gated channels in the cell membrane

Does NOT depend on cell membrane potential

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20
Q

What is the process allowing calcium ion influx into the smooth muscle cytoplasm by pharmacomechanical coupling?

A
  1. Ligands bind to GPCR in cell membrane activating the G protein
  2. Results in activation of phospholipase C
  3. Causes an increase in IP3 and DAG
  4. DAG opens receptor operated Ca2+ ion channels in the cell membrane
  5. IP3 activates calcium ion influx from the SR
  6. Reduced SR calcium ion conc, is sensed by STIM1 in SR which then opens Store-operated Ca2+ channel Orai1 in the cell membrane resulting in more ion influx.
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21
Q

Describe the effect of protein Kinase C on smooth muscle contraction

A

Results in Ca2+ ion dependent smooth muscle cell contraction
Increases the activity of MLCK
Decreases the activity of MLCP
Overall results in a higher proportion of phosphorylated myosin light chains
Increasing muscle contraction

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22
Q

How can the sensitivity of smooth muscle contraction to Ca2+ be modulated?

A

By kinases and/or second messengers
This can decrease the reliance on calcium ion dependent contraction in favour of independent calcium ion contraction

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23
Q

Why is the latch state hypothesis important to the function of smooth muscle contraction?

A

Allows high forces of contraction to be maintained for long periods of time without excessive hydrolysis of ATP
This prevent an extremely elevated metabolic demand helping to avoid fatigue

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24
Q

What is the latch state hypothesis of smooth muscle contraction?

A

When myosin heads already bound to actin are dephosphorylated they enter a latch state
This means they detach slowly from actin, allowing a greater number of cross bridges to be maintained so some cross bridge cycling and ATP hydrolysis can occur
This results in some tention without expending significant ATP
= high tension state by low energy consumption

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25
Q

What is the mechanism behind the latch state hypothesis in smooth muscle?

A

MLCK phosphorylates myosin to activate it and allow it to engage in the cross bridge cycle (ATP activity)
At any stage in this cycle MLCP can act to dephosphorylate myosin inhibiting further progress in the cross bridge cycle - this results in reduced cross bridge cycling and reduced ATPase activity
If this occurs when myosin is bound to actin tension is maintained = latch state hypothesis.

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26
Q

How does ATP contraction and muscle force compare between smooth and skeletal muscle?

A

ATP consumption in smooth muscle it 1/1000 to 1/5000 of striated muscle
Smooth muscle develops force 1000 slower than striated muscle

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27
Q

What are slow waves in the GI tract?

A

Cyclical changes in membrane potential seen in GI smooth muscle cells.
underlie phasic contraction and relaxation

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28
Q

What causes slow waves in the GI tract?

A

Pacemaker currents originating in the interstitial cells of Cajal network.

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29
Q

What evidence shows that Interstitial cells of cajal (ICC) are the pacemakers of smooth muscle contraction?

A

Electrodes recorded a peak in slow waves originating in the ICC always preceeding smooth muscle cell depolarisation

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30
Q

Describe the anatomy of the interstitial cells of cajal? ICC

A

Form a network with each other amongst and between smooth muscle layers

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31
Q

How are ICC, Ca2+ and depolarisation all related?

A

ICC influence depolarisation of smooth muscle cells which allows Ca2+ entry
Note ICCs do not directly cause Ca2+ entry, rather spike potentials are generated from the smooth waves which can then influence calcium ion entry.

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32
Q

What is the resting membrane potential in smooth muscle?

A

-56 millivolts

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33
Q

Describe the relationship between slow waves, spikes and action potentials?

A
  1. Slow waves are baseline and occur all the time - triggered by pacemaker ICC cells
  2. Stimulation (from reflexive activation of stretch receptors/ chemoreceptors or parasympathetic) cause depolarisation
  3. When slow waves occur at a membrane potential more porisitve than -40mv spike potentials appear on the peaks,
  4. The frequency of spikes is proportional to the positivity of the slow wave potential
  5. Spike wave triggers smooth muscle contraction.
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34
Q

What factors can contribute to the depolarisation of the membrane potential?
( slow waves)
What does this lead to?

A

Strethcing of muscle
Acetylcholine (parasympathetic)
Gastroinstetinal hormones - gastrin and motilin

Increased force of contraction and increased frequency of action potentials

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35
Q

What factors contribute to the hyperpolarisation of the membrane potential?
(slow waves)

A

Sympathetic nerve stimulation
Typically noradrenaline and adrenaline

GIT hormone GIP (gastrin inhibitory polypetide) a GIT hormone

Decreases the force of contraction and the frequency of action potentials.

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36
Q

How can slow waves be modulated?

A

Neural and hormonal input
This does not influence the frequency of slow waves, it influences the membrane potential
Hence the frequency of action potentials and the force of contraction.

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37
Q

What is a tonic contraction?
How does it occur in the GIT?

A

Is a weak but a long time maintained isometric contraction
Occurs in smooth muscle cells as subthreshold slow waves can trigger a weak contraction (WITHOUT the occurence of an action potential)

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38
Q

What is a phasic contraction and how can it occur in smooth muscle cells?

A

Phasic contraction - a fast short lived isometric contraction
Occurs when action potential/spike wave is triggered.

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39
Q

How does the affect of repetitive action potential vary between skeletal and smooth muscle?

A

Skeletal - each action potential is followed by a seperate contraction or twitch
smooth - action potentials and twithches summate into sustained contraction

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40
Q

What controls the rate of passage thorugh the GIT?

A

Contraction of sphincters
Changing the rate of peristalsis

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41
Q

Why is it important to be able to control the rate of passage through the GIT?

A

Enzymatic reactions take time
Needs to be able to slow the passage of food to ensure there is plenty of time for this reaction to occur.
This enables time for nutrients to be absorbed across the interstinal wall.

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42
Q

What are the differenct reflexes that control the passage of food through the GIT?

A

Gastroileal reflex
Gastrocoloic?duodenocolic reflexes
Enterogastric reflex
intestinointestinal reflex
Colonioleal reflex

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43
Q

What is the gastroilial relfex?

A

Stomach activity promotes the opening of the ileocaecal sphincter

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44
Q

What is the gastrocolic/duodenocolic reflexes?

A

Food enterting the stomach or duodenum promotes motility of the colon

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45
Q

What is the enterogastric reflex?

A

Distention of the small and large intestinges inhibits stomach motility and secretion

46
Q

What is the intestiniintestinal reflex?

A

Over distation of one part of the intestine leads to relaxation of the rest of the intestine

47
Q

What is the colonoileal reflex?

A

The colon is stretched, inhibits ileal emptying

48
Q

What is achalasia?

A

A disorder when the relaxation of the LES and peristalsis of the oesophagus fails to be triggered after swallowing.
Excitatory neural tone dominates preventing LES relaxation
Thought to be caused by the loss of vasoactive intestinal polypeptide and nitric oxide releasing inhibitory interneurons in the myenteric plexus

49
Q

What are the symptoms of achlasia?

A

Dyshagia
Chest pain
Heartburn
Regurgitation

50
Q

What are the suspected overall pathologies of achalasia?

A

Genetic
Neurodegnerative
Automimmune - activated CD8+ cells and antibodies against the myenteric plexus have been identified in patients

51
Q

What are the treatments for achalasia?

A

Heller myotomy - muscles of the LES are cut to allow food to pass
Botolinum toxin - injected into LES, inhibits excitatory nerves to decrease pressure
Endoscopic pneumatic dilation - endoscopy and ballong dilation to aid controlled tearing of oesophagus to allow food to pass.

52
Q

What systems innervate the GIT?

A

The autonomic nervous system - divided into the extrinsic nervous system and the enteric (intrinsic) NS.
The EnNS acts independently of the CNS and is the main driver of action, the ExNS mainly regulates the activity of the EnNS

53
Q

What plexuses make up the tneric nervous system?
What is there function?

A

Myenteric - controls GI motility
Submucosal plexus - controls GI motility and secretion
Together they function independently of the CNS to stimulate local reflexes in motility and secretion of the GI tract

54
Q

What sort of things does the enteric nervous system regulate?

A

Works independently of the CNS
Has localised effects in the GIT
Affects secretion, motility, gut microcirculation and immunological function

55
Q

What are the effects of the CNS on the GI tract?

A

Influence the GI tract indirecrly via the stimulation of the enteric nervous system
Para - promotes motility and secretion
Symph - inhibits motility/secreton and contracts sphincters
Can connect to sensory receptors and processes from other neurons located both inside and outside the plexus

56
Q

How does the sympathetic CNS system have an affect on the GIT?

A

Originates in preganglionic cholinergic neurons.
These synapse with postganglioninc nodarenergic neurons.
Results in a decreases release of acetylcholine from enteric neurons - inhibits GI motor and secretory function

57
Q

How does the parasympathetic NS have an affect on the GIT?

A

Fibres include the vagus nerve and sacral outflow tracts (pelvic nerve).
Has an indirect effect via the enteric nervous system

58
Q

What are the three different categories of GI peptides?

A

Hormones
Paracrine
Neurocrines

59
Q

What are GI hormones?
Examples

A

Released by endocrine cells of the GI tract
Secreted into portal circulation, then pass into systemic circulation by the liver. Then travel to bind to receptors and have an effect on a target cell at a distant site or within the GI tract.
For example gastrin, CCK, secretin and GIP

60
Q

What are paracrine GI peptides?
Examples

A

Produced by endocrine cells of the GI tract
Travel by local diffusion
To bind to receptors and act on target cells locally within he same tissue
For example somatostain

61
Q

What are neurocrine withint the GIT?

A

Released from neuron of the GIT.
Released after an action potential, they diffuse across the synapse to act on their target cell
For example: Ach, noradrenaline, VIP, enkephalins, NPY and substance P

62
Q

What is the function og Ach as a neurocrine of the ENS?

A

Produced from cholinergic neurons
Causes contraction of smooth muscle in the wall and relexation of sphincteris
Increases salvia, gastric and pancreatic secretion

63
Q

What is the function of noradrenaline as a neurocrine of the ENS?

A

Produced by adrenergic neurons
Causes relaxation of the smooth muscle wall
Contraction of sphincters
And Increase salivary production

64
Q

What is the role of Vasoactive Insteinal Peptide (VIP) as a neurocrine of the ENS?

A

Produces by neurons in the ENS
Relaxaes smooth muscle
Increases intestinal secretion and increases pancreatic secretion

65
Q

What is the tole of NO as a neurocine of the ENS?

A

Produced by neurons int eh ENS
Relaxation of smooth muscle

66
Q

What is the function of Gastrin-Releasing Peptide (GRP) or bombesin as a neurocrin of the ENS?

A

Produced by vagal neurons of the gastric mucosa
Increases gastrin secretion

67
Q

What is the role of enkephalins (opiates) as a neurocrine of the ENS?

A

Produced by neurons of the ENS
Causes contraction of smooth muscle and decrease intestinal secretion

68
Q

What is the role of peptide YY as a neurocrine of the ENS?

A

Produced in the ileum and the colon by enteroendocrine cells
Results in decreases H+ secretion, pancreatic secretion and lower ghrelin.

69
Q

What is the role of neuropeptide Y as a neurocrine of the ENS?

A

Produced by ENS neurons
Causes relaxation of smooth muscle and decreases intestinal secretion

70
Q

What is the role of substance P as a neurocrine of the ENS?

A

Cosecreted with ACh with END neurons
Results in contraction of smooth muscle and increased salivary production

71
Q

What is active relaxation of the stomach in digestion?

A

Relaxation of smooth muscle in the stomach to decreases intraluminal pressure
Occurs after swallowing bolus
This allows large volumes of food to be accommodates with a minimal rise in intragastric pressure

72
Q

What is recepetive relaxation of the stomach?

A

Active relxation occurs first - decreases intraluminal pressure after swallowing of food
Receptive relaxation - food enters stomach and pressure returns to approximately what it was before swallowing

73
Q

What is the purpose of receptive relaxation of the stomach?

A

Allows the stomach to be a temproary food store
Allows time for controlled release of chyme into the duodenum.

74
Q

What is the cause of receptive relaxation in the stomach?

A

Vagovagal reflex
Seratonin receptors cause NO release to relax smooth muscle
Mechanoreceptors detect distention of the stomach and relay to the CNS
Efferent signlans then cause the orad stomach walls to relax by the release of VIP

75
Q

What is gastroparesis?

A

Delayed gastric emptying in the absence of a blockage in the stomach
May be caused by damaged to the vagus nerve affecting peristalsis and parasympathetic outflow to the GIT

76
Q

What are the symptoms of gastroparerisis?

A

Feeling full very quickly when eating
Sickness
Loss of appetite
Weight loss
Bloating
Abdominal pain
Discomfort
Heartburn

77
Q

What is the link between gastroparesis and diabetes?

A

High blood glucose and large fluctuations in blood glucose damages the vagus nerve.
Unable to receive parasympathetic outflow to the GIT

78
Q

What is segmentation of the small intestine?

A

Occurs in the fed state
Is non propagated focal contraction of the intestine at multiple locations simultaneously
Lasts for 4-6hrs following a meal

79
Q

What is the function of segmentation of the small intestine in the fed state?

A

Helps to mix stomach contents, pinch it off into smaller segments and increase contact with digestive enzymes, secretions and mucosa

80
Q

Explain how the ICC and the CNS influence peristalsis?

A

ICC - initiation of, must be present in order for it to occur
ENS - occurrence and force of contraction are dependent on the ENS (which can be influence by the CNS)

81
Q

What is peristalsis?

A

An intrinsic local reflex that helps move food from the GI towards the anus is a propagated fashion.

82
Q

Describe the muscular changes that occur in peristalsis that enables the movement of food through the GIT?

A

Behind (oral end) - contraction of circular and relaxation of longitudinal smooth muscle resulting in narrowing of lumen pushes the bolus forward
Rectal end (in front of ) - relaxation of circular and contraction of longitudinal muscle results in an increased diameter allow the bolus to move into.
This is controlled by inhibitory and exhibitor neurons

83
Q

What is physiological ileus in the GUT?

A

Term to describe the normal absence of motility and propulsion in the small and large intestine.
ENS stimulates quiescient motor functions when no bolus present

84
Q

What triggers peristalsis in the GIT?

A

Chyme causes luminal distention causes direct activation of mechanoreceptive endings on intrinsic primary afferent neurons (IPAN)
Chyme can also be sensed by enteroendocrine cells causing seratonin release which can indirectly activation IPANs

85
Q

What is the role of IPANs (intrinsic primary afferent neurons) in peristalsis?

A

Activate ascending and descending interneurons
Asecinding internuerons then stimulate exicatotry motor neurons
Descending interneurons then stimulate inhibitory motor neurons

86
Q

What substances may be excreted by inhibitory motor neurons?

A

NO
VIP

87
Q

What substances may be secreted by neurons in the submucosal plexus?

A

ACh or VIP

88
Q

What is Hirchsprung disease?

A

Rare condition that causes faeces to become stuck in the bowel.
Mainly effects babies and young children
Nerves that control peristalis are missing from a section of the bowel causing faces to build up and form a blockage
Usually picked up after birth and treated with surgery as soon as possible

89
Q

What are some severe consequences of Hirchsprung disease if it is not treated fast enough?

A

Cause severe constipation and lead to serious bowel infection called enterocolitis.

90
Q

What is the migrating motor complex?

A

A cycle of electrical and motor activity that occurs in the fasting state
Sweeps from the stomach down to the terminal ileum
Cleans and clenses the stomach and SI contents before the next meal
(this may include clearing dead enterocytes and pathogens)

91
Q

What are the three phases of the migrating motor complex?

A

1: quisecence (inactivity)
2: low grade contraction - gherlin secreted from X/A like cells stimulates and maintains through vagal efferent nerves
3: intense contractions - initiated by motilin release from M cells and the direct action of ghrelin on the gut

92
Q

How often is the migrating motor complex activated?

A

Every 60-90 minutes in the interdigestive period

93
Q

What is the effect of the vagus nerve on contractions after a meal?

A

After a meal vagus nerve initiates and maintains contractions

Later motilin-induced contraction are inhibited by the vagus nerve related pathway - this prevents too strong contractions happening too quickly after a meal

94
Q

What is the medical term for emesis?

A

Vomiting

95
Q

What are the different stimuli that can induce vomiting?

A

Pain
Foul Odours
Repulsive sights
Psychological factors

96
Q

What is the area posterma?

A

An area in the brain stem that communicates with the emetic coordinating centre (vomiting centre).
it includes a chemoreceptor trigger zone which detects changes in the levels of chemicals or toxin in the blood to induce nause or vomitting

97
Q

What area of the brain do most anti-emetics block?

A

The area posterma

98
Q

What is the purpose of the vomiting reflex?

A

To clear noxious substances from the stomach before they do damage to the body.

99
Q

What are the different ways that the vomiting centre can be activated?

A

Area posterma - detecting toxins in the blood
Motion sickness caused by unequal vestibular cochlear input
Drugs can trigger the involvement of seratonin receptors on the vaugs nerve (such as in radiation induced vomiting, chemotherapy and postoperative vomiting)
Psychogeneic vomiting can be activated when the higher cerebral cortex interacts with the vomiting centre.
Mechanical stimuli in the GI tract such as irritation of the throat or distention of the stomach

100
Q

What are the common complications of vomitting?

A

Electrolyte and acid-base unbalance
Often suffer from hypokalemia and metabolic alkalosis and gastric juice contains a lot of K+ and H+

101
Q

What is the vomiting centre?

A

Refers to an area of the brain stem involved in the mechanism of autonomic vomiting, this includes the chemical trigger zone and the nucleus of the solitary tract

102
Q

How is the area posterma able to detect chemical changes in order to cause vomiting?

A

In the floor of the fourth ventricle
Lacks blood brain barrier
Can detect systemic stimuli in the blood and CSF through receptors

103
Q

What nucleuses are important in the vomiting centre and what is their function?

A

Nucleus of the solitary tract - recives afferent (sensory input) signals then communicates to the
Dorsal motor nucleus of the vagus - initiates motor output by the vagal efferent nerves to trigger vomiting.

104
Q

What change in the GIT allows the propulsion of food during vomiting?

A
  1. Retroperistalic movement from duodenum into the stomach causing distention of duodenum and relaxation of Pyloric sphincter
  2. Contraction of duodenum/stomach alongside opening of UES
  3. Aided by contraction of abdominal muscles and diaphragm (causing forced expiration)
  4. Rapid increase in intrabdominal pressure and decrease in thoracic pressure
  5. Properls stomach contents out
  6. The larynx moves upward and forward, and the LES relaxes to move food from stomach into O and into mouth
105
Q

What does enteric meaning?

A

Of or relating to the small intestine

106
Q

What structures controls the passage between the ileum and the colon?

A

The ileocecal sphincter
Allows movement in the fed and fasting state

107
Q

What is the purpose of the colon in digestion?

A

Stores faeces until can be defecated conveniently
Allows maximal absorption of water, electrolytes, short-chain fatty acids and bacterial metabolites

108
Q

What causes defecation from the colon?

A

Autonomic control causing mass movement (typically peristalsis under parasympathetic sacral outflow)
Gastrocolic reflex triggered within 30 minutes of a meal - stimulates by CCK release
Peristaltic reflex provides high amplitude and long duration contractions
Mass movement is required in the distal colon as more water absorption makes the fecal content semisolid

109
Q

What structures prevent defecation?

A

Tonic control of the internal anal shincter (smooth muscle under subconscious control)
and the external anal sphcinter (skeletal muscle under conscious control)

110
Q

Describe how skeletal muscle contraction differs to smooth muscle contraction.

A

Smooth: myosin modified by MLCK before engaging in cross cycle
Skeletal; actin binding site modified by Ca2+ binding to tropnin c before can engage in the cross bridge cycle.

Smooth: can occur in a calcium dependent mechanism
Skeleta: requires calcium ions

Smooth: electromechanical and pharmomechanical methods of activation
Skeletal: electromechanical method of activation only.

Unit 10 (37 decks)

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