Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

104 Theme 1 > motility of the GI tract > Flashcards

motility of the GI tract Flashcards

1
Q

what is digestive system

A

GI tract and accessory organs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what is the role of the GI tract

A

Role is to extract chemical energy, vitamins, minerals and water from ingested products
6 processes – ingestion, secretion, motility, mechanical and chemical digestion, absorption and elimination of waste

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what is the basic 4 layer structure of the digestive tract

A

Mucosa
Submucosa
Muscularis Externa
Serosa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How are structural differences linked to variations in primary function

A

same basic structure but
Oesophagus – transport
Stomach – storage, secretion, mixing and digestion
Small intestine – secretion, mixing, majority of digestion, absorption
Large intestine – limited absorption (water, ions), faeces formed, gut microbiota

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what does digestion depend on

A

coordinated motility
Motility is governed by involuntary contraction of smooth muscle with pacemaker interstitial cells of Cajal
Except upper oesophagus and external anal sphincter (striated skeletal muscle, voluntary)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what makes up smooth muscle

A

a single unit – gap junctions allow electrical coupling and contraction as a functional syncytium
organised into connected bundles of outer longitudinal and inner circular smooth muscle in muscularis layer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what does motility occur autonomously with

A

external regulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what does the intrinsic enteric nervous system (ENS) do

A

controls GI motility and secretion independently via 2 interconnected plexuses in gut wall – myenteric and submucosal plexus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

how is the ENS controlled

A 
Extrinsic autonomic – sympathetic and parasympathetic innervation allows central modification
reflex contraction in response to local stimuli (stretch, nutrients, irritation, hormones)
Myenteric plexus (Auerbach’s) in muscularis layer – motility 
Submucosal plexus (Meissner’s) in submucosal layer – secretion and local blood flow
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what is the extrinsic autonomic nervous system (ANS)

A

ANS modifies basal activity of ENS
Parasympathetic innervation – excitatory to motility and secretion (via Vagus and pelvic splanchnic nerves)
Sympathetic innervation – inhibitory to motility and secretion (via thoraco-lumbar innervation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How is GI motility affected by hormones

A

Endocrine hormones are secreted by entero-endocrine cells in the epithelial layer of the GI mucosa and enter portal blood circulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what hormones affect GI motility

A

CCK - pancreatic secretions, gallbladder contractions, growth of exocrine pancreas, inhibits gastric emptying
Motilin - stimulate gastric and intestinal motility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What mechanisms cause contractions?

A

Like all excitable cells smooth muscle cells have a fluctuating negative electrical potential difference across the membrane
Results in two types of electrical activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what are the two types of electrical activity affecting contractions

A

Slow waves – cyclical oscillations of membrane potential spontaneously initiated by pacemaker ICCs
Spike potentials – generated once threshold is reached resulting in Ca2+ influx and smooth muscle contraction
electrophysiology trace - slow wave followed by spike

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Stimulation of smooth muscle contraction

A

Slow waves – basic electrical rhythm

Spike potential – contraction by further depolarisation to threshold levels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

how does depolarisation link to stretch hormones

A 
stretch hormones (motilin), excitatory neurotransmitter Ach release from ENS excitatory motor neurons or P/S
Inhibition by hyperpolarisation caused by inhibitory ENS, sympathetic NT norepinephrine or hormones (secretin)
17
Q

Two types of contraction

A

Segmentation for mixing – bursts of circular muscle contraction and relaxation, back and forth pendular movements also occur
Peristalsis for propulsion – local distension triggers contraction behind bolus and relaxation in-front, waves of contraction, requires functional myenteric plexus, law of the intestines – move aborally

18
Q

result of ENS innervation dysfunction

A

Hirschsprung’s disease
A rare congenital absence of myenteric plexus, usually involving a portion of the distal colon
The pathologic aganglionic section of colon lacks peristalsis and undergoes continuous spasm, leading to functional obstruction and severe constipation

19
Q

3 stages of swallowing (deglutition)

A

Oral – voluntary initiation of swallowing in oral cavity
Pharyngeal – involuntary passage of food through pharynx into oesophagus
Oesophageal – involuntary passage of food from pharynx to stomach
Pressure changes during swallowing

20
Q

what happens during the oral stage of swallowing

A

Voluntary control, tongue pushes up against hard palate and contracts to force lubricated bolus into the pharynx
The pharynx consists of oropharynx, nasopharynx and laryngopharynx
Bolus enters the oropharynx initiating the pharyngeal stage through stimulation of sensory receptors

21
Q

what happens during the pharyngeal stage of swallowing

A

Swallowing centre in medulla oblongata and pons in brain stem (reflex)
Motor efferents in trigeminal, glossopharyngeal and vagal nerves cause series of muscle contractions moving bolus through oropharynx into laryngopharynx and into oesophagus
Soft palette elevates over posterior nares to close nasal pharynx
Epiglottis closes larynx
Respiration inhibited
Upper oesophageal sphincter relaxes
Pharyngeal muscle contraction propels bolus into oesophagus

22
Q

what happens during the oesophageal stage of swallowing

A

Primary peristalsis moves bolus downwards
Circular muscle contracts behind bolus, longitudinal muscle contracts in front to shorten fibres and push wall outwards
Mucus lubricates and reduces friction
Relaxation of lower oesophagus and lower oesophageal sphincter occurs
Secondary peristalsis stimulated by stretch
Coordination is via intrinsic myenteric and extrinsic vagal innervation

23
Q

result of oesophageal motility dysfunction

A

Achalasia
LOS fails to relax so food remains in oesophagus, may be vagal or myenteric defect. Causes distension, inflammation, infection and ulceration
Gastro-oesophageal reflux
LOS tone lost leading to flow of acidic gastric contents into oesophagus (inflammation and ulceration), may be linked to hiatus hernia

24
Q

Stomach 3 primary motor functions

A

Storage – the vagovagal reflex mediates receptive relaxation reducing muscle tone and allowing reservoir function
Mixing – fragmentation of food and mixing with secreted gastric juice for digestion
Emptying contents into duodenum at controlled rate

25
Q

how does the stomach empty

A

high regulated with primary inhibitory feedback signals from small intestine
More powerful peristaltic contractions build to force chyme into duodenum

26
Q

how is the stomach emptying regulated

A

Excitatory – ENS/ANS neuronal stimulation and hormones eg motilin
Inhibitory – ANS regulation, duodenal enterogastric reflexes and hormones eg CCK and secretin
ANS/ENS reduction in gastric emptying

27
Q

Gastric motility dysfunction

Dumping syndrome

A

rapid emptying of gastric contents into small intestine
occurs following ingestion of large meal after gastrectomy
characterised by nausea, pallor, sweating, cramps, vertigo, fainting
may be caused by hypertonic duodenal contents causing rapid entrance of fluid

28
Q

Gastric motility dysfunction

gastroparesis

A

stomach fails to empty
prevents proper digestion
causes bloating and nausea
may be caused by gastric cancer or peptic ulcers
occasionally observed through impaired vagal stimulation to stomach in severely diabetic patients who develop autonomic neuropathy

29
Q

what does the small intestine do

A

motility patterns allow the majority of digestion and absorption of nutrients over 3.5 hours
large SA for absorption provided by circular folds (plicae circulares), villi and microvilli on epithelial apical surface

30
Q

two types of motility in SI

A

mixing and circulation for maximum exposure to absorptive epithelium
propulsion of chyme aborally

31
Q

how is motility controlled in the small intestine

A

controlled by intrinsic motor patterns modified by hormonal and ANS neural stimuli
segmentation for mixing
stretch receptors trigger myenteric stimulation of muscle contraction, no net movement
propulsive peristalsis
stretch, hormones (excitation – gastrin, CCK, insulin, motilin, serotonin and inhibition – secretin and glucagon)

32
Q

propulsive peristaltic reflexes

A

gastroenteric reflex – gastric distension activates myenteric plexus to promote SI peristalsis
gastroileal reflex – gastric distension promotes peristalsis in the ileum to force chyme through ileocecal valve into caecum
migrating motor complex – series of peristaltic contractions, between meals, every 90 mins sweeps into colon. Intrinsic enteric control, hormone motilin. Absence can lead to bacterial overgrowth.

33
Q

Disruption to peristalsis

A

Peristaltic rush – mucosal irritation, ENS and ANS neural reflexes rapidly sweep contents of SI into colon
Paralytic ileus – loss of peristalsis following mechanical trauma
Vomiting – reverse peristalsis initiated in distal SI to expel intestinal and gastric contents

34
Q

what does the large intestine do

A

Motility more sluggish to allow optimal absorption of water and electrolytes (proximal), formation and storage of faeces (distal) and commensal microbiome aids digestion, synthesises B and K vitamins
Longitudinal muscle in muscularis thickened to form 3 bands, taniae coli, which tonically contract to form haustral bulges

35
Q

how is motility controlled in the large intestine

A

Motility is via mixing and propulsion under intrinsic enteric control modified by neural and hormonal stimuli
Mixing contraction via haustral churning

36
Q

how does peristalsis occur in the large intestine

A

mass movements (2/3x per day, forceful peristaltic contractions force contents into sigmoid colon and rectum) and gastro-colic and duodeno-colic reflexes (mass movements occur after meals on stretching via ANS)

37
Q

what is the defecation reflex

A

Initiates defecation to expel faeces containing residues to digestion, bacteria, bile pigment and mucosal debris

38
Q

how does the defecation reflex occur

A

Mass movements push faecal matter into empty rectum
Stretch receptors are stimulated and activate the ENS and PS ANS
Involuntary contraction of longitudinal muscle in rectum opens the internal anal sphincter
The constricted external anal sphincter is voluntarily relaxed to allow defecation

104 Theme 1 (18 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions