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Medicine Unit 10 UoS > GI motility > Flashcards

GI motility Flashcards

1
Q

What is the structure of the GI tract wall?

A

Mucosal layer - epithelium, lamina propria (CT), muscularis mucosae
Submucosal layer - collagen, elastin, glands, blood vessels
Muscularis mucosae - smooth muscle cells - oblique, circular, longitudinal
Serosa

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2
Q

Smooth muscle in the GI tract

A
  • Non-striated muscle cells type - not orderly arranged in sarcomeres
  • Actin = thin filaments
  • Myosin = thick filaments
  • Intermediate filaments (desmin and dense bodies) anchor points for contractile filaments
  • Specialised for long term contraction using little ATP
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3
Q

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

A

Ca2+ conc in the cytosolic fluid of smooth increases due to influx of calcium
Ca2+ bin reversibly to calmodulin (CaM) = calmodulin-calcium complex
CCM joins and activates myosin light chain kinase (MLCK)
One light chain of each myosin head is phosphorylated in response to myosin kinase
- The head has capability of binding repetitively with the actin filament
- Causes muscle contraction and ATP consumption

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4
Q

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

A

When Ca2+ levels fall, kinase becomes inactive, activity of MLCP dominates
Myosin P is dephosphorylated = muscle relaxes

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5
Q

Electromechanical coupling

A

Membrane depolarisation opens the voltage gated Ca2+ channels causing rise in intracellular Ca2+

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6
Q

Pharmacomechanical coupling

A

Ca2+ levels rise from SR and enter via non-voltage gated channels
Chemicals bind to membrane receptors and activate G protein
PLC activation increases concentration of IP3 and DAG - initiates rise in concentration of Ca2+
STIM1 is a Ca2+ sensor that activates store operated Ca2+ channels

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7
Q

When may Ca2+ independent contraction occur?

A

Increase in rate of myosin phosphorylation by MLCK
or
from decrease in rate of myosin dephosphorylation by MLCP

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8
Q

What is the latch state hypothesis?

A

Smooth muscle can maintain high force at low rate of ATP hydrolysis - reduce fatigue
Dephosphorylating myosin already on actin reduces off rate = latch state
Decreased detachment rate increases cross bridge no., lower rate of cross bridge cycling and ATP hydrolysis = low energy consumption/high tension state
After Ca2+ return to normal, smooth muscle retain some tension without spending high ATP

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9
Q

Slow waves in smooth muscle

A

Cyclical changes in membrane potential that underlie phasic contraction and relaxation
originate from interstitial cells of cajal (ICCs) network
Precede events in smooth muscle

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10
Q

What are the roles of ICCs?

A

ICCs (interstitial cells of cajal)
Act as electrical pacemakers
Cells form network through smooth muscle layers
Pacemaker activity cause slow waves which influence depolarisation leading to Ca2+

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11
Q

What is the rate of passage through the GI tract controlled by?

A

Contraction of sphincters
Changing rate of peristalsis

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12
Q

What reflexes occur in the GI tract that controls passage of food? (5)

A

Gastroileal reflex - stomach activity promotes opening of ileocaecal sphincter
Gastrocolic/duodenocolic reflexes - food entering the stomach stomach/duodenum promotes motility of colon
Enterogastric reflex - distension of SI/LI inhibits stomach motility and secretion
Intestinointestinal reflex - over distention of one part of intestine leads to relaxation of the rest of the intestine
Colonoileal reflex - inhibits ileal emptying when colon is stretched

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13
Q

What is achalasia?

A
  • Failure of oesophageal peristalsis and relaxation of the LOS in response to swallowing
  • Symptoms: dysphagia, chest pain, heart burn, regurgitation
  • Caused by loss of vasoactive intestinal polypeptide (VIP) and nitric oxide-releasing inhibitory interneurons in the myenteric plexus
  • Excitatory neural tone dominates, preventing LOS relaxation
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14
Q

ENS (4)

A

Enteric nervous system
Myenteric plexus controls GI motility
Submucosal plexus controls both GI motility and secretion
Can work independently to elicit local reflexes -> changes in motility or secretion

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15
Q

CNS role in GI tract (3)

A

CNS can act indirectly on GI via ENS
Parasympathetic - promotes motility/secretion
Sympathetic - inhibits motility/secretion and contracts sphincters
- originates in preganglionic cholinergic neurons
- decrease release of ACh from enteric neurons = inhibits motility/secretion

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16
Q

What are the different types of GI peptides? (3)

A

Hormones: secreted by endocrine cell, portal circulation, liver, systematic circulation, target cell
Paracrines: act locally within same tissue
Neurocrines: released after AP, diffuse across synaptic cleft -> target cell

17
Q

What role does ACh have in the GI system? (5)

A
  • Contraction of smooth muscle in wall
  • Relaxation of sphincters
  • Increased salivation
  • Increased gastric secretion
  • Increased pancreatic secretion
18
Q

What are the roles of NE in the GI tract? (3)

A
  • Relaxation of smooth muscle in wall
  • Contraction of sphincters
  • Increased salivary secretion
19
Q

What are the roles of VIP in the GI tract? (3)

A

-Relaxation of smooth muscle
- Increased intestinal secretion
- Increased pancreatic secretion

20
Q

What are the role of neuropeptide Y? (2)

A
  • Relaxation of smooth muscle
  • Increased intestinal secretion
21
Q

What are the role of peptide YY? (3)

A
  • Decreased gastric H+ secretion
  • Decreased pancreatic secretion
  • Decreased Ghrelin (decreased appetite)
22
Q

What occurs during receptive relaxation of the stomach? (3)

A
  • Active relaxation of the smooth muscle -> intraluminal pressures fall before bolus arrives
  • Relaxation occurs with each swallow, large volumes can be accommodated without rise of intragastric pressure
  • After passage of bolus, pressure returns to normal = receptive relaxation
23
Q

What does receptive relaxation of the stomach allow? (2)

A
  • Stomach to be a temporary food store
  • Allows time for controlled release of chyme into duodenum
24
Q

How is receptive relaxation mediated? (2)

A
  • Vasovagal reflex - act through serotonin receptors to release NO to cause muscle relaxation
  • Mechanoreceptors detect distention > relay to CNS > efferent information to smooth muscle wall of the orad stomach > relaxation
25
Q

What is gastroparesis? (3)

A
  • Delayed gastric emptying without any blockage in the stomach
  • Symptoms: satiety, bloating, nausea, vomiting
  • Cause by vagal injury > reduced strength of stomach contraction and failure of pyloric sphincter to effectively relax
26
Q

What is segmentation?
Duration?
Function?
(4)

A
  • Small intestinal motility - non-propagated focal contractions of intestine occurring simultaneously
  • Different regions of circular muscle of the gut contract to pinch off lengths of contents
  • Lasts 4-6 hours after eating
  • Mixes contents of GI with digestive secretions and brings them into contact with the mucosa aswell as contractions of villi and muscularis mucosa
27
Q

What is peristalsis?

A
  • Intrinsic local reflex that moves food through the GI tract towards the anus
28
Q

How peristalsis carried out?

A

Orchestrated by interstitial cells of Cajal
CNS can also elicit effects through stimulation of the ENS
- Excitatory neurons cause longitudinal muscle in segment ahead of bolus to contract
- Inhibitory neurons cause circular muscles layer to relax in same segment > expansion of lumen
- Excitatory neurons cause contraction of circular muscle layer in segment behind bolus
- Inhibitory neurons cause relaxation of longitudinal muscle layer in same segment > propulsion of contents

29
Q

What stimulates motor neuron activity in peristalsis? (5)

A

Luminal distention triggers
- direct activation of mechanoreceptive endings of intrinsic primary afferent neurons (IPANs)
- Indirect activation of IPANs upon serotonin release from enterochromaffin cells in the epithelium
IPANs activate
- ascending interneurons > stimulate excitatory motor neurons
- descending interneurons > stimulate inhibitory motor neurons
Motor neuron activity > propulsion of contents proximal-distal direction

30
Q

What is Hirschsprung’s disease?

A

No migration of neurons of the myenteric plexus into the rectum = faeces become stuck

31
Q

What is the migrating motor complex? (5)

A

-Cycle of electrical and motor activity that occurs in the fasting state from the stomach down to the terminal ileum
- Clears the stomach and SI contents before next meal
3 Phases
1: Quiescence (inactivity)
2: Low grade contractions - ghrelin stimulates and maintains through vagal efferent nerves
3: intense contractions - elicited by motilin, ghrelin also acts on stomach and initiates gastrcic phase 3 contractions

32
Q

What neurological structures are involved to lead to nausea and vomiting? (3)

A

Stimuli converge on neurons located in emetic centre in medulla
Chemoreceptor trigger zone within the area postrema allows chemical changes in blood to induce nausea and vomiting
Antiemetics will block the signalling here

33
Q

What stimuli can induce vomiting? (6)

A
  • Pain
  • Foul odours
  • Food poisoning
  • Cancer chemotherapy
  • Pregnancy sickness
  • Psychological factors
34
Q

What muscular changes lead to vomiting? (5)

A
  • Retroperistaltic response moves food from duodenum back into the stomach (distension of duodenum, pyloric sphincter and stomach relaxes to accomodate)
  • Contractions in duodenum and stomach
  • Contraction of skeletal muscle - abdo wall and downward contraction of diaphragm > squeezes stomach between diaphragm and abdo muscles > forced inspiration
  • Increased in abdo pressure and decrease in thoracic pressure, propels stomach contents out
  • Movement of larynx up and forward and relaxation of upper and lower oes sphincter > allows contents from stomach through oes and mouth
35
Q

Describe the movement of contents through the colon (5)

A
  • Entry controlled by ileocecal sphincter continuously
  • Contents pushed by mass movement under autonomic control (initiated by stimulation of parasympathetic sacral outflow tracts)
  • Gastrocolic reflex increases colonic motility within 30 min of a meal - neurally mediated by CCK release
  • Giant peristaltic contraction = peristaltic reflex = high amplitude and long duration contractions
  • Contents semisolid in distal colon, harder to move, final mass movement propels contents into rectum
36
Q

What is defacation controlled by?

A

Prevented by tonic contraction of internal and external anal sphincters
- Internal = smooth muscle - subconsciously controlled
- External = skeletal muscle - voluntarily controlled

Medicine Unit 10 UoS (26 decks)

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