Swallowing, Gastric Emptying and Intestinal Motility

Question 1

Phases of swallowing

Answer 1

oral, pharyngeal, esophageal

Question 2

Aspects of gastric motility

Answer 2

Receptive relaxation/Gastric accommodation, Mixing, Emptying, Migrating myoelectric complex

Question 3

small intestine motility (3)

Answer 3

Segmentation, Peristalsis, Migrating myoelectric complex

Question 4

large intestine motility (4)

Answer 4

Haustrations, Long-duration contractions, Mass movements

Defecation reflex

Question 5

Swallowing: receptors, integration center, effectors

Answer 5

Deglutition
Initiated voluntarily

Reflex control of events moving food from mouth → stomach
Receptors: Touch receptors
-Primarily near opening of pharynx
Integration center: Swallowing center
-Medulla oblongata (lower pons)
Effectors: Pharyngeal and esophageal striated and smooth m.
-Cranial n.n.: pharynx and upper esophagus
-Vagus n.: lower esophagus

Question 6

Swallowing: 3 Phases

Answer 6

Oral phase: Voluntary
-Bolus: tongue  pharynx

2. Pharyngeal phase: Involuntary
   -Initiated by response to pressure
   receptors in pharynx
   -Directs bolus into esophagus via
   relaxed upper esophageal sphincter (UES)
3. Esophageal phase: Involuntary
   -Bolus from UES via peristalsis through
   lower esophageal sphincter (LES)  stomach

Question 7

Pharynx propulsive function

Answer 7

food transfer to esophagus

Question 8

Upper Esophageal Sphincter (UES) propulsive functions and protective effects

Answer 8

allows entry of food into esophagus

protects airway from swallowed material

Question 9

Esophagus function and protective effects

Answer 9

transports bolus from pharynx to stomach

clears material refluxed from stomach

Question 10

Lower Esophageal Sphincter (LES) function and protective effects

Answer 10

allows entry of food into stomach

protects esophagus from gastric reflux

Question 11

Swallowing- oral phase

Answer 11

Tongue pushes bolus against hard palate

Touch receptors of the pharynx detect bolus
Swallowing reflex is initiated

Question 12

Swallowing- pharyngeal phase

Answer 12

involuntary

Propels food from pharynx into esophagus
Respiration inhibited
1.Bolus is directed into pharynx
-Elevation of soft palate blocks entry
to nasopharynx
2.Epiglottis blocks entry to trachea
3.Pharyngeal m.m. push bolus into pharynx; UES relaxes
4.Peristaltic wave moves bolus
through UES
5. During pharyngeal stage of swallowing, respiration is
reflexely inhibited

Question 13

Pressure peak travels during swallowing

Answer 13

pharynx -> upper sphincter of esophagus –> junction of smooth and striated muscle–> body of esophagus–> lower sphincter of esophagus

Question 14

Swallowing: esophageal phase

Answer 14

After UES closes, LES begins to relax
Primary peristaltic wave begins below UES
-Reflex initiated by swallowing
  center
Secondary peristalsis
-Initiated by distention
-Occurs only if primary wave is not
  sufficient

Question 15

What kind of input modulates esophageal peristalsis?

Answer 15

Input from esophageal sensory fibers to the CNS
and ENS modulates both primary and secondary
esophageal peristalsis

Question 16

Sphincters- general

Answer 16

Muscular barriers
High resting pressure in order to maintain separation
Regulate antegrade and retrograde movement
In general:
Proximal stimuli → relaxation
Distal stimuli → contraction
Facilitate unidirectional movement through G.I. tract
Coordination of:
-Other smooth muscle contractions
-Neural stimulation
-Humoral stimulation

Question 17

Sphincters- general

Answer 17

Muscular barriers
High resting pressure in order to maintain separation
Regulate antegrade and retrograde movement
In general:
Proximal stimuli → relaxation
Distal stimuli → contraction
Facilitate unidirectional movement through G.I. tract
Coordination of:
-Other smooth muscle contractions
-Neural stimulation
-Humoral stimulation

Question 18

Upper esophageal sphincter

Answer 18

Skeletal muscle
Regulated by swallowing center via cranial n.n.
Highest resting pressure of GI sphincters
Closed during inspiration
Limits air entry to esophagus

Question 19

Lower esophageal sphincter

Answer 19

Smooth muscle
Primary function:
allows coordinated movement of food into stomach
prevents reflux of gastric contents into esophagus
LES resting tone:
-Intrinsic myogenic properties
-Cholinergic regulation
LES relaxation:
Intrinsic smooth muscle properties
Vagus n. (inhibition by VIP and NO)
LES relaxation occurs after UES returns to resting pressure
Swallowing or esophageal distention → decreases LES pressure

Question 20

GERD

Answer 20

the most common symptom of
heartburn due to stomach acid reflux
into esophagus
is not a disease but a normal physiological process
stomach contents leak backwards from the stomach into the esophagus and irritates the lining of the esophagus
this occurs when the lower esophageal sphincter (LES) does not work properly
weak squamous lining of the lower esophageal section
decrease secretion of mucus and bicarbonate in saliva

Question 21

Barrett’s esophagus

Answer 21

(pre-cancerous lesion):

it is most often diagnosed in people who have long-term GERD (chronic inflammation)
this condition is recognized as a complication of GERD
a condition in whichcolumnar cells replace squamous cell in themucosa of esophagus
the main cause of Barrett’s esophagus is thought to be an adaptation to chronic acid
exposure fromreflux esophagitis
its importance lies in its predisposition to evolve into esophagealcancer
it develops in about 10–20% of patients withchronic GERD.

Question 22

Dysphagia

Answer 22

common problem in elderly people with difficulty
in swallowing, food getting caught in esophagus
risk of aspiration, choking and malnutrition
difficulty in swallowing due to abnormalities in:
structural - anatomical structures
- abnormal tongue, cannot propel bolus backward
- diverticula (outpouchings of pharyngeal or
esophageal wall) in which food is trapped.
functional - abnormal swallowing reflex
- neurological defect and control of oropharyngeal
swallowing, peristalsis, and esophageal sphincter
relaxation, or to defects in muscle layers.
disease state:
- neurological disorders
- stroke
- Parkinson’s disease
- myasthenia gravis
- xerostomia

Question 23

Achalasia

Answer 23

(failure to relax):
special form of dysphagia
complete lack of peristalsis within esophagus
LES does not relax and increased LES pressure
food is retained at the level of LES
caused by:
- nerve degeneration (enteric nervous system)
- lack of NO synthase, VIP, etc
- Chagas disease (infection protozoa: Trypanosoma cruzi)

Question 24

What does the radiography look like in achalasia?

Answer 24

bird’s beak

Question 25

Incompetent LES

Answer 25

The LES acts like a guard that prevents anything that gets into the stomach from refluxing into the esophagus, it acts as a pressure barrier at the gastro-esophageal junction Incompetent LES or transient relaxation of LES are the most common symptoms of reflux. Physiologically, a well functioning LES will remain closed except in: - primary peristalsis-within 2 sec after a swallow, leads to LES relaxation for 5-10 sec (release of NO & VIP) and then contracts - secondary peristalsis-LES relaxation occurs as a reflex after distention of proximal striated or more distal esophageal smooth muscle - transient LES relaxation are not associated with pharyngeal contraction or esophageal peristalsis and persists for more than 10 sec. control of LES function are not completely understood various drugs, hormones, and neuro-humoral agents produce stimulatory or inhibitory effects on the LES by binding with specific receptors cessation of excitatory cholinergic activity and release of NO and VIP leads to LES relaxation GERD is secondary to an incompetent lower esophageal sphincter as the real cause to incompetent LES is not known it is sometimes referred to as idiopathic LES Incompetence

Question 26

Diffuse esophageal spasms

Answer 26

diffuse esophageal spasms (DES) are irregular, uncoordinated, and sometimes powerful contractions of the esophagus it is characterized by contractions that are of normal amplitude but are uncoordinated, simultaneous, or rapidly propagated these spasms can prevent food from reaching the stomach, leaving it stuck in the esophagus it can cause dysphagia, regurgitation and chest pain the cause of esophageal spasm is unknown may caused by disruption of the nerve activity that coordinates the swallowing action of the esophagus in some people, very hot or very cold foods may trigger an episode

Question 27

What does radiography look like in DES?

Answer 27

corkscrew appearance

Question 28

Hiatal hernia

Answer 28

a hiatus hernia or hiatal hernia is the protrusion (or herniation) of the upper part of the stomach into the thorax through a tear or weakness in the diaphragm in hiatal hernia, it is easier for stomach acids to come up into the esophagus this causes a burning feeling in the throat and chest symptoms similar to GERD

Question 29

Functional divisions of the stomach: roles in motility

Answer 29

LES and Cardia: prevention of reflux, entry of food, regulation of belching Fundus and body: reservoir, tonic force during emptying Antrum and pylorus: mixing, grinding, sieving, regulation of emptying

Question 30

Receptive relaxation

Answer 30

Initiated by swallowing (esophageal peristalsis) LES and stomach (fundus & body) relax Vagovagal reflex Vasoactive Intestinal Peptide (VIP) Pressure in stomach does not increase despite increased volume Disruption of vagus n. → rapid pressure increase Vagotomy

Question 31

Gastric accomodation

Answer 31

Relaxation in response to gastric filling -Activate dilation of fundus Early changes in volume do not result in increased gastric pressure -Allows for storage After threshold: rapid increase in pressure for increased volume Vagus n. -Modulates -Vagotomy results in decreased accommodation Enteric nervous system

Question 32

Overview: gastric mixing and emptying- Excitatory portion

Answer 32

Excitatory: Gastric Mixing (Antrum) Increased gastric contractility Stomach contents: (+) stimuli for increasing contractility -Volume of chyme (distension) - Fluidity of chyme ENS: Acetylcholine and Substance P Gastrin

Question 33

Gastric mixing and emptying: inhibitory portion

Answer 33

Inhibitory: Gastric Emptying Duodenum contents: (-) stimuli for gastric emptying -Duodenum has to be ready to receive food -Stimuli in duodenum inhibit gastric emptying: Fatty acids & monoglycerides; Acidic pH; Volume/distension, Hypertonicity, Amino acids & peptides Neural responses: Intrinsic & extrinsic Hormonal response: Cholecystokinin (CCK), Secretin, Gastric Inhibitory Peptide (GIP)

Question 34

Effects on gastric motility and emptying: volume of chyme

Answer 34

increased volume stimulates motility and emptying

Question 35

Effects on gastric motility and emptying: degree of fluidity

Answer 35

increased fluidity allows more rapid emptying

Question 36

Effects on gastric motility and emptying: presence of fat, acid, hypertonicity or distension (in duodenum)

Answer 36

these factors in the duodenum inhibit further gastric motility and emptying until the duodenum has coped with factors already present

Question 37

Effects on gastric motility and emptying: emotion

Answer 37

stimulates or inhibits motility and emptying

Question 38

Gastric contractions: Slow waves, APs, pacemaker

Answer 38

``` Pacemaker zone: sets rate of gastric peristalsis -Body of stomach ~ 3 – 5 slow waves/min. Contraction force: -Degree of depolarization -Duration of membrane depolarization Acetylcholine & Gastrin -Increase amplitude and duration -Increase contractility Norepinephrine -Decreases contractility ```

Question 39

Gastric contractions: Slow waves, APs, pacemaker

Answer 39

``` Pacemaker zone: sets rate of gastric peristalsis -Body of stomach ~ 3 – 5 slow waves/min. Contraction force: -Degree of depolarization -Duration of membrane depolarization Acetylcholine & Gastrin -Increase amplitude and duration -Increase contractility Norepinephrine -Decreases contractility ```

Question 40

Gastric Mixing

Answer 40

Propulsion Grinding Retropulsion Trituration: -reduction of solid particle size -> 2 mm do not leave the stomach during the gastric phase (right after a meal) -Emptying is delayed until solids are mechanically broken down

Question 41

Gastric Emptying rates

Answer 41

Liquid > Carbohydrate > Protein > Fat | Isotonic > hypertonic or hypotonic

Question 42

Duodenal contents affecting gastric emptying

Answer 42

Receptors in duodenum: - pH, osmolarity, fatty acids/monoglycerides, amino acids/peptides Gastric emptying slowed by: - Byproducts of fat and protein digestion - Hypertonic chyme -

Question 43

Duodenal contents delaying gastric emptying: coordinated events

Answer 43

Coordinated Events (Neural and Hormonal): Relaxation of the fundus Inhibition of antral contractions Stimulation pyloric sphincter contractions (phasic)

Question 44

Pyloric Sphincter (hormonal and neural regulation)

Answer 44

Hormonal Regulation: Increased constriction: -CCK, GIP, Secretin, Gastrin Neural Regulation: Sympathetic → constriction Parasympathetic: Vagus n. - Constriction: Acetylcholine - Relaxation: VIP

Question 45

Migrating Myoelectic complex: Stomach

Answer 45

``` Fasting State -occurs every 75 – 90 (120) min -starts about 2 hrs after meal Stomach → ileum -“Cleans” tract -Removes remaining ingested contents (solids > 2mm) Burst of antral electrical activity (~ 5-10 min) Very strong antral contractions Relaxation of pylorus ```

Question 46

Vomiting

Answer 46

Complex reflex reaction (Emesis) -Integration includes medullary “vomiting center” Stimuli include: - Gastric & duodenal distention, irritants - Dizziness, inner ear dysfunction, motion sickness - Drugs - Genitourinary injury - Emetics: chemicals that can cause vomiting Chemoreceptor trigger zone (brain 4th ventricle) Gastric/Duodenal receptors (ex: ipecac)

Question 47

Reflex response of vomiting

Answer 47

``` Reverse peristalsis (small intestine → pylorus) Pyloric sphincter relaxes, stomach relaxes Abdominal m.m. contraction Pylorus and antrum contract LES relaxes Gastric contents → esophagus UES relaxes -Retching: UES remains closed ```

Question 48

3 Primary Types of Small Intestinal Motility

Answer 48

Segmentation: -Mixing Peristalsis -Propulsion Migrating myoelectric complex -Sweeping of undigested contents during fasting state

Question 49

Small intestine: 1. Segmentation

Answer 49

Postprandial period: - Alternating contractions of circular smooth m. ``` Slow process of propulsion & retropulsion - Time for digestion & absorption - Mixes chyme with digestive secretions - Maximizes contact with mucosal layer ```

Question 50

Small intestine: 3. Migrating Myoelectric Complex

Answer 50

Propulsive movement initiated during fasting Moves undigested material: Stomach & small intestine → colon New wave starts in stomach once previous wave passes distal ileum Pylorus and ileocecal sphincter are relaxed 3 phases: Quiescence, small disorganized contractions, strong propagating contractions (~ 5-10 min) Repeats every ~ 75-120 min during fasting Correlated with high levels of circulating motilin (small intestinal hormone) Prevents backflow of bacteria from colon into ileum

Question 51

Small intestine: 3. Migrating Myoelectric Complex

Answer 51

Propulsive movement initiated during fasting Moves undigested material: Stomach & small intestine → colon New wave starts in stomach once previous wave passes distal ileum Pylorus and ileocecal sphincter are relaxed 3 phases: Quiescence, small disorganized contractions, strong propagating contractions (~ 5-10 min) Repeats every ~ 75-120 min during fasting Correlated with high levels of circulating motilin (small intestinal hormone) Prevents backflow of bacteria from colon into ileum

Question 52

Basic electrical rhythm of intestinal contractions

Answer 52

slow waves - Duodenum (highest rate: ~ 11-13/min) - Jejunum (~10-11/min) - Ileum (~8-9/min)

Question 53

What to bursts of APs on top of slow waves do?

Answer 53

``` increase strength of contractions for intestinal motility - Hormones - Enteric nerve plexuses - Parasympathetic and Sympathetic via ENS ```

Question 54

Law of intestine:

Answer 54

contraction behind & relaxation in front of bolus | - Intrinsic reflex (ENS)

Question 55

intestinointestinal reflex

Answer 55

: distention in one segment, relaxation in the rest of the small intestine - Long range coordination: Extrinsic and intrinsic ~ 2-4 hrs. for chyme to move through small intestine

Question 56

Ileocecal sphincter

Answer 56

``` Normally contracted Tone coordinated primarily by: - Enteric neural reflexes - Long-range extrinsic neural reflexes - Hormones Distention in ileum → relaxation Distention in ascending colon → constriction Gastroileal reflex - Increased gastric activity → increased ileal motility and relaxation of sphincter ``` Goal: control rate of chyme entering colon so that colon can effectively absorb water and salts

Question 57

3 types of colonic motility

Answer 57

haustrations long-duration contractions mass movements

Question 58

Haustrations

Answer 58

Short-duration contractions (~ 8 sec stationary pressure waves) Circular m. mixing contractions (not propulsive)

Question 59

Long-duration contractions (~ 20-60 sec)

Answer 59

Taeniae coli Mixing contractions, may propagate short distances in either direction Antipropulsive movements in proximal colon: retain chyme Goal: slow movement through colon for absorption

Question 60

Mass movements

Answer 60

High-amplitude propagating contractions (high intensity) Sweep length of colon (cecum to rectum) 1-3/day (1-10/day) High variability in colonic motility rates among individuals (vs. small intestinal motility)

Question 61

Regulation of colonic motility

Answer 61

Primarily neural regulation (ENS, PNS, SNS) Intrinsic control; Extrinsic modulation ``` Local reflexes: Colonic distention Contraction behind (ACH and Substance P) and relaxation (VIP and NO) in front of bolus ``` Long-range reflex: Gastric distention Gastrocolic reflex Stomach distention results in generalized increase in colonic motility

Question 62

ANS regulation of colonic motility

Answer 62

Parasympathetic: increased motility Vagus n. via ENS: Increased mixing contractions in proximal colon Pelvic n.n. via ENS: Increased contractions and propulsive movements in distal colon Sympathetic: Inhibits motility Postganglionics via abdominal sympathetic ganglia

Question 63

Internal anal sphincter

Answer 63

Internal anal sphincter (IAS): Smooth muscle Involuntary control Majority of tone

Question 64

extrenal anal sphincter

Answer 64

Striated muscle | Voluntary & involuntary control

Question 65

Defecation reflex

Answer 65

``` Expulsion of undigestible residues Requires extrinsic neural input – Higher CNS & spinal cord coordination via pelvic n.n. Distention of rectum → Reflex relaxation of IAS Rectosphincteric reflex: VIP & NO Reflex constriction of EAS Postponed defecation: Accommodation of rectum IAS: contract EAS: relax ```

Question 66

Defecation definition

Answer 66

Coordinated series of voluntary and involuntary events including: Voluntary relaxation of EAS Contraction of abdominal m.m. Relaxation of pelvic muscles

Question 67

Hirschsprung's Disease

Answer 67

disease (congenital megacolon) Congenital failure of enteric neural plexus development Impair motility function Aganglionic segment, remains contracted -Commonly just above the IAS becomes dilated Rectosphincteric reflex impaired -Dilation of colon proximal to site of obstruction Treatment: Symptoms alleviated by surgical excision of the diseased segment

Question 68

Irritable Bowel Syndrome

Answer 68

Irritable Bowel Syndrome or Disease (IBS/IBD) is a group of inflammatory conditions of the colon and small intestine. Due to visceral hypersensitivity due to sensitization of afferent neural pathways -respond abnormally to stimuli -idiopathic, distension, inflammation, GI infections, etc -Partially dysmotility The major types of IBD are Crohn’s disease and ulcerative colitis Although very different diseases, may present any of the following symptoms: Abdominal pain, vomiting, diarrhea, rectal bleeding, severe internal cramps Diagnosis by assessment of inflammatory markers is stool followed by colonoscopy with biopsy of pathological lesions.