Phys: Swallowing, Gastric emptying, Intestinal Motility Flashcards
1
Q
3 phases of swallowing
A
- Oral phase: Voluntary
- Bolus: tongue pharynx
- Pharyngeal phase: Involuntary
-Initiated by response to pressure
receptors in pharynx
-Directs bolus into esophagus via
relaxed upper esophageal sphincter (UES) - Esophageal phase: Involuntary
-Bolus from UES via peristalsis through
lower esophageal sphincter (LES) stomach
2
Q
Oral phase
A
- voluntary
- Tongue pushes bolus against hard palate
- Touch receptors of the pharynx detect bolus
- Swallowing reflex is initiated
3
Q
Pharyngeal phase
A
- Propels food from pharynx into esophagus
- Respiration inhibited
- Bolus is directed into pharynx. Elevation of soft palate blocks entry to nasopharynx
- Epiglottis blocks entry to trachea
- Pharyngeal m.m. push bolus into pharynx; UES relaxes
- Peristaltic wave moves bolus through UES
- 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.
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
5
Q
swallowing
A
- induces peristaltic wave of constriction through esophagus, relaxation then contraction of LES, and relaxation of stomach
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
7
Q
UES
A
upper esophageal spincter
- striated muscle, regulated by swallowing center via cranial nn.
- highest resting pressure
- closed during inspiration
8
Q
esophagus muscle make up
A
1/3 striated muscle
2/3 striated + smooth muscle
3/3 smooth muscle
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
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
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
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
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
14
Q
Orad region:
A
- Fundus and body
- luminal secretion: HCl, IF
- resevoir, provides tonic force during emptying
15
Q
Caudad region
A
- antrum and pylorus
- helps with mixing, grinding , sieving, regulation of emptying
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
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
18
Q
VAgotomy
A
cutting of vagus n.
- results in decreased gastric accomodation and less relaxation
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
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
21
Q
What three things inhibits gastric emptying
A
CCK, Secretin, GIP
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
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
gastric emptying
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
Gastric mixing
- 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
What slows gastric emptying?
- 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
Acidic Chyme
- Neural and hormonal response
Secretin:
- -> Decreased contractility in antrum
- -> Increased constriction of the pylorus
29
Fatty acids and/or monoglycerides....
-Neural and hormonal response
Cholecystokinin and Gastric Inhibitory Peptide
- ->Relaxation of gastric smooth muscle
- ->Increased constriction of the pylorus
30
Peptides and AA's
Hormonal response
Gastrin:
- Increased contractility in antrum
- Increased constriction of pylorus
Overall effect? too slow of emptying
31
Pyloric sphincter constriction????
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
MMC
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
Vomiting
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
Segmentation of SI
- mixing of chyme allowing slow process for absorption
35
Peristalsis
- propulsion - not mixing - propelling down tract
36
Segmentation in fed state after eating
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
Peristalsis in fed state after eating
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
postprandial
during or relating to the period after dinner or lunch.
39
why does peristalsis occur?
It is a response to stretch
Excitatory: release ACh and Substance P for contraction
Inhibitory: release NO, VIP for relaxation
40
Electrical rhtyhm
- Duodenum (highest rate: ~ 11-13/min)
- Jejunum (~10-11/min)
- Ileum (~8-9/min)
41
Law of Intestine
```
contraction behind & relaxation in front of bolus
Intrinsic reflex (ENS)
relaxation caused by VIP and NO (*important*)
```
42
Intestinointestinal reflex
distention in one segment = relaxation in the rest of the small intestine
43
feeding vs. fasting state
MMC is active during fasting.
| During feeding state, segmental contractions and peristaltic contractions occur.
44
Ileocecal sphincter
- normally contracted
- distension in ielum --> relaxation
- distension in ascending colon --> constriction
45
Gastroileal reflex
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
1. Colonic motility: Haustrations
- 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
2. Colic motility: Long duration contractions
- 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
3. Colic motility: Mass movements
- 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
contraction, relaxation of colon
Colonic distension: Contraction behind (ACH and Substance P) and relaxation (VIP and NO) in front of bolus
50
PS stimulation of colon
- 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
Sympathetic stimulation of colon
- inhibits motility
Postganglionics via abdominal sympathetic ganglia
52
Internal anal sphincter (IAS)
- smooth muscle, involuntary control, majority of sphincter tone comes from here
53
External anal sphincter (EAS)
- striated m, voluntary and involuntary control
54
Hirshsprungs disease
= 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
Irritable Bowel Syndrome
- 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.
