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GI test 2 > Phys: Swallowing, Gastric emptying, Intestinal Motility > Flashcards

Phys: Swallowing, Gastric emptying, Intestinal Motility Flashcards

1
Q

3 phases of swallowing

A
  1. 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
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2
Q

Oral phase

A
  • voluntary
  • Tongue pushes bolus against hard palate
  • Touch receptors of the pharynx detect bolus
  • Swallowing reflex is initiated
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3
Q

Pharyngeal phase

A
  • 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

–> tongue thrusts up and back at same time nasopharynx closes - bolus moves through pharynx and UES as larynx elevates, airway closes, UES opens and pharynx contracts.

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4
Q

Esophageal phase

A

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
  • Input from esophageal sensory fibers to the CNS
    and ENS modulates both primary and secondary
    esophageal peristalsis
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5
Q

swallowing

A
  • induces peristaltic wave of constriction through esophagus, relaxation then contraction of LES, and relaxation of stomach
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6
Q

sphincters

A
  • maintain a high resting pressure in order to regulate antegrade and retrograde movement

in general:

  • proximal stimuli –> relaxation
  • distal stimuli –> contraction
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7
Q

UES

A

upper esophageal spincter

  • striated muscle, regulated by swallowing center via cranial nn.
  • highest resting pressure
  • closed during inspiration
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8
Q

esophagus muscle make up

A

1/3 striated muscle
2/3 striated + smooth muscle
3/3 smooth muscle

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9
Q

LES

A
  • remains high level of tone to prevent GERD
  • function: coordinated mvmt of food into stomach, prevents gastric reflux into esophagus
  • LES resting tone maintained by intrinsic myogenic properties and ACh
  • LES constriction = ACh, Substance P = excitatory
  • LES relaxation = VIP, NO- sphincter is open. without these it will remain constricted the whole time
  • swallowing/esophageal distension –> decreases LES pressure < intragastric pressure –> allows food entry into stomach
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10
Q

Timing of UES and LES Relaxation

A
  • Timing of UES & LES Relaxation Promotes Unidirectional Movement
  • Timing and pressure are important for unidirectional mvmt
  • Both sphincters are not open at the same time
  • When this tone is not maintained, cannot swallow
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11
Q

Achalasia

A
  • dysphagia = difficulty swallowing due to absence of smooth m. relaxation
  • dilated esophagus proximal to LES, but LES fails to relax. Due to peristalsis impairment in the smooth m. portion of esophagus. Loss of inhibatory VIP and NO innervation.
  • treatment: use balloon to force open
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12
Q

GERD

A
  • Gastroesophageal Reflux Disease
  • usually LES resting pressure prevents gastric contents from refluxing into esophagus
  • A reduction of LES resting pressure → gastroesophageal reflux
  • Gastric juice results in Esophagitis or erosion of the esophageal mucosa
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13
Q

regions of stomach

A

“orad region” = fundus and proximal body - receives and stores food

“Caudad region” = distal body and antrum - mixing and propelling

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14
Q

Orad region:

A
  • Fundus and body
  • luminal secretion: HCl, IF
  • resevoir, provides tonic force during emptying
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15
Q

Caudad region

A
  • antrum and pylorus

- helps with mixing, grinding , sieving, regulation of emptying

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16
Q

Receptive relaxation

A

= anticipated relaxation

  • initated by swallowing and esophageal peristalsis
  • causes LES and stomach (fundus and body) to relax.
  • Vagus mediated response
  • Pressure in stomach does not increase
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17
Q

Gastric Acommodation

A
  • relaxation in response to gastric filling - activated by dilation of fundus.
  • early changes in volume do not result in increased gastric pressure which allows for storage.
  • after threshold has been reached, rapid increase in pressure occurs
  • Vagus n: modulates relaxation
  • ENS: important in reflex relaxation
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18
Q

VAgotomy

A

cutting of vagus n.

- results in decreased gastric accomodation and less relaxation

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19
Q

factors causing increased motility/emptying of stomach…..

A

+ Gastrin secreted from G cells results in increased gastric contractility/emptying

+ ACh and Substance P from ENS result in contraction of stomach

  • increased volume of chyme (distension) and fluidity of chyme are also positive stimuli for stomach contraction and emptying
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20
Q

factors causing decreased motility/emptying of stomach…..

A
  • contents in duodenum inhibit gastric emptying. the duodenum must be able to receive food.
  • stimuli in duodenum such as FA’s, monoglycerides, Acidic pH, volume/distension, AA’s and peptides all inhibit stomach emptying

Hormonal response:
CCK, Secretin, GIP

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21
Q

What three things inhibits gastric emptying

A

CCK, Secretin, GIP

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22
Q

Interstitial Cells of Cajal

A
  • pacemaker that set rate of gastric peristalsis
  • 3-5 slow waves/min
  • contraction force due to degree of depolarization and duration of membrane potential
  • ACh and Gastrin: increase amplitude, duration and contractility of APs
  • NE: decreases contractility
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23
Q

ACh, Gastrin

A
  • depolarize membrane so AP can be reached easily

- increase amplitude, duration and contractility of stomach contractions

24
Q

NE

A
  • hyperpolarize membrane so there is no threshold for contraction
  • decreases stomach contraction
25
Q

gastric emptying

A
  1. peristaltic contraction originates in upper fundus and sweeps down toward pyloric sphincter
  2. contraction becomes more vigorous as it reaches thick-muscled antrum
  3. strong antral peristaltic contraction propels chyme forward
  4. small amount of chyme is pushed through sphincter into duodenum
26
Q

Gastric mixing

A
  • propulsion, grinding, retropulsion
  • trituration (reduction of solid particle size) occurs due to propulsion of bolus toward pylorus, grinding due to material being funneled through a small opening and retropulsion of fluid moving back.
27
Q

What slows gastric emptying?

A
  • byproducts of fat and protein digestion, hypertonic chyme and pH less than 3.5: results in coordination of gastric emptying with duodenum to ensure chyme can be effectively processed by duodenum and is not regurtiated back into stomach
  • results in relaxation of fundus, inhibition of antral contractions, contraction of pyloric sphincter
28
Q

Acidic Chyme

A
  • Neural and hormonal response

Secretin:

  • -> Decreased contractility in antrum
  • -> Increased constriction of the pylorus
29
Q

Fatty acids and/or monoglycerides….

A

-Neural and hormonal response

Cholecystokinin and Gastric Inhibitory Peptide

  • ->Relaxation of gastric smooth muscle
  • ->Increased constriction of the pylorus
30
Q

Peptides and AA’s

A

Hormonal response

Gastrin:
- Increased contractility in antrum
- Increased constriction of pylorus
Overall effect? too slow of emptying

31
Q

Pyloric sphincter constriction????

A

Hormonal regulation: increased constriction due to CCK, GIP, Secretin, Gastrin

Neural Regulation:

  • sympathetic –> constriction (halts food processing)
  • PS (via Vagus n.): ACh results in constrction for additional mixing. VIP results in relaxation for emptying
32
Q

MMC

A

Migrating Myoelectric Complex

  • occurs during fasting state (every 25-90 mins), also starts 2 hrs after meal.
  • contraction moving from stomach –> ileum to clean the tract and remove remaining ingested contents
  • burst of strong antral electrical activity
  • relaxation of pylorus
  • occurs in both stomach and GIT
  • present in fasting state for sweeping and cleaning effect
  • correlated with high levels of MOTILIN
  • prevents backflow of bacteria from colon into ileum
33
Q

Vomiting

A

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
Reflex response: 
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

34
Q

Segmentation of SI

A
  • mixing of chyme allowing slow process for absorption
35
Q

Peristalsis

A
  • propulsion - not mixing - propelling down tract
36
Q

Segmentation in fed state after eating

A
  1. postprandial period: alternating contractions of circular smooth m allows for segementation
    2 slow process of propulsion and retropulsion: allows for further segmentation and time for digestion and absorption. mixes chyme with digestive secretions. maximizes contact with mucosal layer.
37
Q

Peristalsis in fed state after eating

A

Postprandial: coordinated propulsive contractions of circular smooth m.

  • relaxation in front of bolus due to VIP and NO
  • Contraction behind bolus from ACh and Substance P
38
Q

postprandial

A

during or relating to the period after dinner or lunch.

39
Q

why does peristalsis occur?

A

It is a response to stretch
Excitatory: release ACh and Substance P for contraction
Inhibitory: release NO, VIP for relaxation

40
Q

Electrical rhtyhm

A
  • Duodenum (highest rate: ~ 11-13/min)
  • Jejunum (~10-11/min)
  • Ileum (~8-9/min)
41
Q

Law of Intestine

A 
contraction behind & relaxation in front of bolus
Intrinsic reflex (ENS)
relaxation caused by VIP and NO (*important*)
42
Q

Intestinointestinal reflex

A

distention in one segment = relaxation in the rest of the small intestine

43
Q

feeding vs. fasting state

A

MMC is active during fasting.

During feeding state, segmental contractions and peristaltic contractions occur.

44
Q

Ileocecal sphincter

A
  • normally contracted
  • distension in ielum –> relaxation
  • distension in ascending colon –> constriction
45
Q

Gastroileal reflex

A

increased gastric activity –> increased ileal motility and relaxation of sphincter

Goal: to control rate of chyme entering colon so that colon can effectively absorb water and salts

46
Q
  1. Colonic motility: Haustrations
A
  • Short-duration contractions (~ 8 sec stationary pressure waves)
  • Circular m. mixing contractions (not propulsive)
  • slower alternate contractions for water and salt absorption, than in SI, this is because we need to reabsorb as much water as possible
47
Q
  1. Colic motility: Long duration contractions
A
  • Long-duration contractions (~ 20-60 sec): due to longitudinal muscles 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
48
Q
  1. Colic motility: Mass movements
A
  • 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 which results in some people getting constipation
49
Q

contraction, relaxation of colon

A

Colonic distension: Contraction behind (ACH and Substance P) and relaxation (VIP and NO) in front of bolus

50
Q

PS stimulation of colon

A
  • increases motility

Vagus n. via ENS: Increased mixing contractions in proximal colon

Pelvic n.n. via ENS: Increased contractions and propulsive movements in distal colon

51
Q

Sympathetic stimulation of colon

A
  • inhibits motility

Postganglionics via abdominal sympathetic ganglia

52
Q

Internal anal sphincter (IAS)

A
  • smooth muscle, involuntary control, majority of sphincter tone comes from here
53
Q

External anal sphincter (EAS)

A
  • striated m, voluntary and involuntary control
54
Q

Hirshsprungs disease

A

= congenital megacolon: due to failure of enteric neural plexus development

  • impairs colon motility function, aganglionic segment above IAS remains contracted and becomes dilated
  • diseased portion of colon must be removed surgically
55
Q

Irritable Bowel Syndrome

A
  • inflammation of colon/small intestine
  • Due to visceral hypersensitivity due to sensitization of afferent neural pathways
  • 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.

GI test 2 (14 decks)

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