Lecture 19 Flashcards

1
Q

Segmentation in small intestine?

A

Allows full contact of contents with intestinal juices for digestion and the intestinal wall for absorption.

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2
Q

Skeletal muscle?

A

Found only in the upper third of the oesophagus (and lower part of large intestine) and contraction is under voluntary control.

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3
Q

Smooth muscle?

A

Found in rest of GI Tract (majority) where contraction occurs in response to neuronal and hormonal or paracrine input.

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4
Q

How do skeletal muscles contract?

A

Must be stimulated by neurons. Motor neurons innervate skeletal muscle via axons branching and forming junctions with the muscle. Axon terminals contain vesicles which in turn contain neurotransmitter.

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5
Q

Neurotransmitter junction?

A

Action potential in motor neurone leads to Ach (acetylcholine) release at cleft between motor end plate and muscle. ACh binds to receptors on motor end plate (muscle plasma membrane under axon terminal), opening ion channels and resulting in depolarisation.

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6
Q

EC coupling in skeletal muscle?

A

Need increase in calcium -> enables calcium release from intracellular stores, then binds to troponin -> to cause muscle contraction. Removal of Ca2+ from the cytosol is required for relaxation.

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7
Q

What type of muscle is in small/large intestine?

A

Smooth

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8
Q

Excitatory/inhibitory neurotransmitters?

A

A neurotransmitter can be either excitatory or inhibitory to smooth muscle contraction. N.B. Skeletal muscle receives only excitatory input

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9
Q

EC coupling in smooth muscle?

A

Different mechanism – no troponin involved. Instead, contractile proteins are regulated by Ca2+/Calmodulin activation of Myosin Light Chain Kinase resulting in phosphorylation of myosin -> contraction

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10
Q

Excitatory neurotransmitter?

A

Lead to contraction (e.g. acetylcholine ACH)

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11
Q

Inhibitory neurotransmitter?

A

Lead to relaxation (e.g. VIP)

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12
Q

What is contraction of smooth muscle regulated by?

A

Neurotransmitters released by autonomic nerve endings. No specialised motor end plate but swollen axon regions (varicosities) containing NT.
Can also be regulated by hormonal or mechanical input via receptor activation.

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13
Q

Electrically coupled?

A

Connected by gap junctions so are electrically coupled (changes in one affects it’s neighbours) e.g. smooth muscle cells

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14
Q

Transit in duodenum?

A

Is rapid, slowing down as chyme progresses through the small intestine. Most digestion and absorption occurs in the duodenum and jejunum.

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15
Q

Transit in ileum?

A

Rate of absorption is slower in the ileum and transit time is also slower. This allows absorption of more slowly digested substances e.g. fats, bile, fat-soluble vitamins

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16
Q

Fed state?

A

Fed condition produces random motor activity of sequential contractions (segmentation). Physical nature of the food affects the number of contractions. Solid food induces twice as many contractions as equicalorific liquid. Carbohydrates > protein > lipid

17
Q

Fasted state?

A

Interdigestive peristaltic activity occurs (known as the migrating myoelectic complex (MMC) and begins in the stomach). As one complex reaches the ileum, another starts at the stomach again. This moves undigested material towards the large intestine.

18
Q

What the MMC initiated by?

A

An increase in the hormone motilin which increases neuronal activity

19
Q

Disorders that cause faster transit time?

A

Diarrhoea, IBS, chronic pancreatitis

20
Q

Disorders that cause slower transit time?

A

Constipation, diabetes, partial gastrectomy (removal of stomach)

21
Q

Therapies of GI dysmotility

A

Anti-spasmodics - reduces muscle contraction (Buscopan)
Anti-motility - decrease activity of myenteric plexus (loperamide)
Prokinetics - increase contraction (Tegaserod)
Laxatives - stimulate intestinal movement by increasing bulk/adding lubrication/acting as local irritant