Control of smooth muscle in the GI tract Flashcards

1
Q

What are the types of muscle in the GIT

A

Smooth (involuntary) muscle in most regions

Skeletal (voluntary) muscle in the pharynx top third of the oesophagus, external anal sphincter

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2
Q

What are the functions of the GIT

A

digestion
absorption
secretion
motility

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3
Q

What are the two types of smooth muscle?

A

Phasic - rapid relaxation and contraction of the muscle

Tonic - muscle remains contracted or relaxed for a long duration of time

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4
Q

what are the interstitial cells of CAJAL (ICC)

A

Pacemaker cells which have a spontaneous oscillating membrane potential. These cells are electrically coupled to the smooth muscle cells through gap junctions.

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5
Q

What can cause stimulation of electrical activity of smooth muscles in the GIT? (depolarisation)

A

stretch
acetylcholine
parasympathetics

Initiates smooth muscle contraction

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6
Q

What can cause hyperpolarisation of smooth muscles in the GIT?

A

Noradrenaline
sympathetics

Initiates smooth muscle relaxation

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7
Q

What is the role of Ca2+ ions in smooth muscle contraction?

A

Ca ions bind to calmodulin which activates myosin light chain kinase enzyme when phosphorylates myosin, allowing it to interact with actin and therefore mediates contraction.

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8
Q

How does relaxation occur in smooth muscle?

A

MLCP phosphatase dephosphorylates myosin so it no longer interacts with actin molecules and hence contraction is halted.

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9
Q

How is Ca controlled to control contraction?

A

Ca ions are exchanged by a Na-Ca exchanger of Ca pump, but this eventually would deplete the cell of Ca ions.
Instead Ca ions re-uptake into the sarcoplasmic reticulum

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10
Q

How can relaxation of smooth muscle be maintained?

A

MLCP can itself be phosphorylated meaning that it cannot interact with calmodulin and as such no muscle contraction will be cause

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11
Q

What does activation of the myenteric plexus do?

A

Increases tonic contraction
increases intensity of rhythmic contractions
increases the rate of rhythmic contractions
increases velocity of conduction

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12
Q

What does activation of the submucosal plexus do?

A

Involved primarily with the absorptive function of the GIT

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13
Q

What are the different types of movements in the GIT?

A

A.Propulsive movements: PERISTALSIS

B.Non-propulsive movements: SEGMENTATION

C.Interdigestive: MIGRATING MOTOR COMPLEX (MMC)

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14
Q

What sensory receptors are involved in the GIT?

A

Enteric sensory neurones

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15
Q

What are the roles of the para/symp NS in motility of the GIT?

A

Sympathetic inhibits motility

Parasympathetic initiates motility

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16
Q

What type of reflexes are involved in the gut wall?

A

Ileogastric
gastrocolic
enterogastric

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17
Q

What is the Gastro colic reflex?

A

sensory distension initiating a reflex of contractions in the large intestine allowing more room for new food in the colon.

18
Q

What is the intestine intestinal reflex?

A

(inhibitory reflex)

prevents excess chyme being secreted into the ileum when distention hasn’t been fully completed

19
Q

What is Hirschsprung disease?

A

Congenital lack of neuronal ganglionic cells in the ENS leading to a lack of motility and therefore can cause MEGAcolon

20
Q

What is Chagas disease?

A

infectious disease of a parasitic nature, resulting in the significant reduction in the number of ganglionic cells in the ENS

21
Q

What is Achalasia?

A

a condition in which the muscles of the lower part of the oesophagus fail to relax, preventing food from passing into the stomach caused by a dramatic reduction in the number of neuronal cells in the lower oesophageal segment.

22
Q

What are some gastric functions of the stomach?

A

gastric emptying/release
Food storage
gastric motility and mixing

23
Q

How is the stomach adapted for storage function?

A

Can be highly folded and upon filling the folds flatten out allowing an increase in volume.
Once the stomach folds extend fully (via the vago-vagal reflex) then the intraluminal pressure increases and it becomes harder to eat.

24
Q

what are the phases of gastric motility in the stomach?

A

Propulsion - rapid flow of liquids and suspended small particles are pushed down towards the pylorus.
Grinding - the emptying of liquids and small particles but larger particles are retained in the bolus and are subject to grinding.
Retropulsion - this is where large particles are cleared in the terminal antrum

25
Q

What is the function of the pylorus?

A

allows carful regulated emptying of gastric contents

prevents regurgitation of duodenal contents

26
Q

What are the phases of gastric emptying?

A

– Cephalic - approach of food or food in the mouth
– Gastric - food in the stomach
– Intestinal - food in duodenum, ileum or colon

27
Q

What occurs during the cephalic phase of gastric emptying?

A

An inhibitory phase - Inhibitory nerve fibres in the vagus nerve
Results in relaxation of stomach enabling it to store large volumes

28
Q

What occurs during the gastric phase of gastric emptying?

A

Is an excitatory phase in which the stomach empties at rate proportional to the volume in it.

29
Q

What occurs during the intestinal phase of gastric emptying?

A

It is (mainly) an inhibitory phase, through which the duodenum adapts the “work-load” as a function of the state of the digestive process.

30
Q

what is the predominant excitatory neurotransmitter for smooth muscle control?

A

ACh

31
Q

What is the predominant inhibitory neurotransmitter for smooth muscle control?

A

VIP and NO

32
Q

Which fibre inhibits and stimulates motility by controlling the resting membrane potential?

A

Stimulation of membrane potential by Sympathetic fibres inhibit motility
Stimulation of membrane potential by parasympathetic fibres increases motility.

33
Q

What are the symptoms of Hirschsprung disease?

A

Vomiting
constipation
distension of abdomen
Intestinal obstruction

34
Q

What patient evaluation takes place to diagnose Hirschsprung’s disease?

A

plain abdominal radiography
Rectal manometry
Biopsy

35
Q

What is the treatment for Hirschsprung’s Disease?

A

Removal of Aganglionic segment and subsequent anastomosis

36
Q

What is the clinical presentation of Achalasia?

A
Solid Dysphagia (difficulty swallowing)
Chest pain
Regurgitation
Pyrosis
Weight loss
Nocturnal cough and recurrent aspiration.
37
Q

What is the diagnosis of Achalasia?

A

Plain film
Barium esophagogram
Endoscopy
Oesophagal manometry

38
Q

What is the treatment for Achalasia?

A

Nitrates and Calcium Channel Blockers
Botulinum toxic preventing ACh release at NMJ
Pneumatic dilation
Surgical myotomy.

39
Q

What causes the emptying of the stomach during the gastric phase of

A

Myogenic reflex: stretching smooth muscle causes reflex contraction
Activation of pressure receptors which send impulses in local nerve plexi and in the vagus nerve
Gastrin released in response to peptides etc

40
Q

What controls the intestinal phase of gastric emptying?

A

This phase is mainly controlled through hormonal and paracrine mechanisms, activated by duodenal chemoreception.

There are also some motor reflexes such as ileogastric reflex delaying gastric emptying

41
Q

What are the intestinal mechanisms controlled by hormonal and paracrine mechanisms?

A

Low pH - activates secretion of Secretin
High fats/lipids - increase secretion of CCK
High levels of amino acids - increase secretion of Gastrin
High levels of carbohydrates - increased secretion of GIP

42
Q

What is the significance of The intestinal phase of gastric emptying being inhibitory?

A

delays gastric emptying increasing the time taken for the GI tract to empty and thus allow more time for digestion.