Motility of the GI Tract Lecture (TEST 2) Flashcards
Motility is one of the Major Activities taking place in the GI Tract
- Motility involves the Contraction and Relaxation of the Walls and Sphincters of the GI Tract
Motility is key for:
1) Preparation of Ingested Food or Digestion and Absorption (Grinds, Mixes, and Fragments Foods)
2) Propelling ingested food from the mouth toward the Rectum
- Motility rate is regulates along the GI Tract
The Circular and Longitudinal Muscle of the GI Tract have different Functions
- CIRCULAR MUSCE Contraction DECREASES the DIAMETER of the Segment
- LONGITUDINAL MUSCLE Contraction DECREASES the LENGTH of the Segment
Phasic and Tonic Contractions of Smooth muscle are Key for Motility along the GI Tract
PHASIC CONTRACTION:
- Periodic Contractions followed by Relaxation
- Esophagus, Stomach (Antrum), Small Intestine, and all tissues involved in Mixing and Propulsion
TONIC CONTRACTION:
- Maintain a Constant level of Contraction WITHOUT Regular periods of Relaxation
- Stomach (Orad), Lower Esophagus, Ileocecal, and Internal Anal Sphincter
Slow waves are Unique feature of the GI Smooth Muscle
- SLOW WAVES are Depolarization and Repolarization of the Membrane Potential
- APs occur when the DEPOLARIZATION moves the Membrane Potential to or above the THRESHOLD
- The Mechanical Response (Contraction or Tension) follows the Electrical Response
- Frequency of Slow Waves varies along the GI Tract (3 to 12 waves/ min)
Relationship between Slow Waves, APs, and Contractions in the Smooth Muscle
- In GI Smooth Muscle even Subthreshold Depolarization can produce weak Contraction (BASAL CONTRACTION)
- The Greater the Number of APs on top of the Slow Wave the LARGER the PHASIC CONTRACTION
- **ACETYLCHOLINE = INCREASES the Amplitude of Slow Waves and the Number of APs
- Stretch, Acetylcholine, Parasympathetic
- **NE = DECREASES the Amplitude of Slow Waves
- Norepinephrine, Sympathetics
Interstitial Cells of Cajal are the Pacemaker for GI Smooth Muscle
- Slow Waves ORIGINATE in the INTERSTITIAL CELLS of CAJAL (ICC)
- Slow Waves occur spontaneously in the ICC and spread RAPIDLY to Smooth Muscle via GAP JUNCTIONS
- Electrical Activity in the ICC drives the FREQUENCY of CONTRACTION!!!
Swallowing is Initiated VOLUNTARILY in the Mouth, and after that it is under INVOLUNTARY REFLEX CONTROL
Three Phases of Swallowing:
1) ORAL PHASE:
- Initiates Swallowing Process
2) PHARYNGEAL PHASE:
- Passage of Food through Pharynx into Esophagus
- Soft Palate is pulled UPWARD —> Epiglottis moves —> UES Relaxes —-> Peristaltic Wave of Contractions is initiated in Pharynx —> Food is propelled through open UES
3) ESOPHAGEAL PHASE:
- Passage of Food from Pharynx to Stomach
- Controlled by the Swallowing Reflex and the ENS
a) Primary Peristaltic Wave
b) Secondary Peristaltic Wave
The Involuntary Swallowing Reflex is Controlled by the Medulla
- Swallowing Center is located in the MEDULLA
- Food in the Pharynx —-> AFFERENT Sensory Input vis VAGUS/ GLOSSOPHARYNGEAL Nerve ——> Swallowing Center (Medullar) ——> Brain Stem Nuclei —> EFFERENT Input to PHARYNX
- The Swallowing Center INHIBITS the RESPIRATORY CENTER During the PHARYNGEAL Stage
During the Esophageal Phase there are two types of Peristaltic Waves
1) PRIMARY Peristaltic Wave:
- Continuation of Pharyngeal Peristalsis
- Controlled by the Medulla (Swallowing Center)
- Cannot occur after VAGOTOMY
2) SECONDARY Peristaltic Wave:
- Occurs if Primary Contraction FAILS to EMPTY the Esophagus or when Gastric Contents REFLUX into the Esophagus
- Induced by DISTENTION
- Repeats until Bolus is Cleared
- Both swallowing Center and ENS are Involved
- Can occur in the ABSENCE of Oral and Pharyngeal Phases
- Occurs EVEN AFTER VAGOTOMY!!!!!!
During Swallowing there are Changes in pressure along the Esophagus as Food Bolus Passes through it
- MANOMETRIC Readings from the Esophagus and Stomach show the Changes in INTRALUMINAL PRESSURE BETWEEN SWALLOWS and DURING SWALLOWING
Esophageal Pressure
BETWEEN SWALLOWS:
BETWEEN SWALLOWS:
- Both the UES and the LES are Closed
- The Body of the Esophagus is FLACCID
- The Pressure in the UES > PHARYNX and Body of Esophagus (~ 60 mmHg)
- LES also exhibits elevated Pressure (20 to 40 mmHg)
- Pressures in the Body of the Esophagus are SIMILAR to those within the Body cavity in which the Esophagus lies
a) In the THORAX the Pressure are SUBATOMSPHERJC and VARY WITH RESPIRATION
b) FLUCTUATIONS in Pressure with Respiration REVERSE Below the Diaphragm
c) INTRALUMINAL Esophageal Pressure reflects Intra-Abdominal Pressure
The Intrathorvacic Location of the Esophagus poses a Challenge
TWO PROBLEMS:
1) Keeping AIR OUT of the Esophagus at the Upper End
2) Keeping ACIDIC GASTIC Contents OUT of the Lower End
How Problems are Solved?
- Both UES and LES are Closed, except when Food Bolus is passing from Pharynx to Esophagus or from Esophagus to Stomach
**GASTROESOPHAGEAL Reflux occurs when Intra-abdominal Pressure is INCREASED!!!
Esophageal pressures
DURING SWALLOWS:
DURING SWALLOWS:
- UES Relaxes (Opens = LOW PRESSURE)
- Once the Bolus Passes, the Sphincter CLOSES and assumes its Resting Tone
- PERISTALTIC WAVE (Body of the Esophagus undergoes Peristaltic Contraction = HIGH PRESSURE)
- LES and Upper Part of the Stomach RELAX = RECEPTIVE RELAXATION (Low Pressure
- Opening of LES mediated by PEPTIDERGIC FIBERS In the VAGAL NERVE
a) Vagal Input is INHIBITORY
b) Release of VASOINTESTINAL PEPTIDE (VIP)
c) Role of NITRIC OXIDE (NO) a Neurotransmitter involved in Relaxation of LES has been also Proposed - Receptive Relaxation DECREASES the Pressure in the Upper Region of the Stomach
- After Bolus ENTERS Stomach, LES Contracts (INCREASE Pressure)
Gastroesophageal Reflex Disease
- Heartburn/ Acid Indigestion (1/10 People)
- Backwash of Acid, Pepsin, and Bile into Esophagus (Abnormal Relaxation of the LES)
Some SYMPTOMS:
a) Heartburn
b) Chest Pain
c) Difficulty Swallowing (DYSPHAGIA)
d) Regurgitation of Food (Acid Reflux)
e) Sensation of a lump on your Throat, Dry Cough, Etc.
Can LEAD TO:
a) STRICTURE of Esophagus (Scar Tissue)
b) ASTHMA (Aspiration)
c) Chronic Sinus INFECTION (Reflux in Throat)
d) BARRETT’S ESOPHAGUS!!!!!!!
Achalasia
- Greater than 200,000 cases in the US per year
- NEUROGENIC ESOPHAGEAL MOTILITY DISORDER
a) Impaired Peristalsis
b) Lack of LES Relaxation during Swallowing. The LES Stays CLOSED DURING SWALLOWING, resulting in the back up of Food (Causes: LACK of VIP or ENTERIC SYSTEM has been KNOCKED OUT)
c) Elevation of LES RESTING PRESSURE - Results from damage to NERVES in the Esophagus, preventing it from SQUEEZING Food into the Stomach
- May be caused by an ABNORMAL IMMUNE SYSTEM RESPONSE
SYMPTOMS: Backflow of Food in the Throat (Regurgitation), Difficulty Swallowing (Dysphagia), Vomiting, Chest Pain, Heart Burn, and Weight Loss
TREATMENT: ENDOSCOPIC Therapy or Surgery
The Stomach can be Regionally dived according to DIFFERENCES in Motility in, Addition to its Anatomical Divisions
Anatomical Divisions:
- Fundus
- Body
- Antrum
Two Regions:
- Orad
- Caudad
- A Particularity of the Stomach: It has 3 LAYERS OF MUSCLE:
a) Circular
b) Longitudinal
c) Oblique - EXTRINSIC Innervation: ANS!!!!!!!
- INTRINSIC Innervation: MYENTERIC and SUBMUCOSAL Plexus!!!!!!!
Receptive Relaxation occurs in the ORAD Region of the Stomach
- Th Function of RECEPTIVE RELAXATION is to receive the FOOD BOLUS in the Stomach
RECEPTIVE RELAXATION: DECREASE Pressure and INCREASE Volume of the Orad Region
- Receptive Relaxation is a VASOVAGAL REFLEX!!!!!
- The ORad Exhibits minimal Contractile Activity therefore little mixing of Ingested Food occurs in this region of the Stomach
- CCK DECREASES Contractions and INCREASES Gastric Distenstibility
Mix and Digestion occur in the Caudad Region of the Stomach
- Contractions of the CAUDAD Region of the Stomach serve to both MIX and PROPEL Gastric Contents
- The Primary CONTRACTILE EVENT is PERISTALTIC CONTRACTION (Mid Stomach —> Pylorus)
- AS Contractions approach the pylorus, they INCREASE in BOTH FORCE and VELOCITY
- Max Frequency is ~ 3 to 5 Waves Per Min
- **In the CAUDAD Region, most of the Gastric Contents are PROPELLED BACK into the Stomach for FURTHER MIXING and FURTHER REDUCTION of Particle Size (RETROPULSION!!!!!!!)
- Wave of Contraction closes the Pylorus
- Peristaltic Waves moves from mid Stomach to Antrum
There is NO NET MOVEMENT of Gastric Contents between CONTRACTIONS!!!!**
Regulation of Gastric Contractions
PARASYMPATHETIC Stimulation, GASTRIN, and MOTILIN
- INCREASE AP and Force of Contractions
SYMPATHETIC Stimulation, SECRETIN, and GIP
- DECREASE AP and Force of Contractions
Gastric Emptying is accomplished by coordinated Contractile Activity of the Stomach, Pylorus, and Proximal Small Intestine
Rate of Gastric Emptying is INCREASED By:
a) DECREASED Distensibility of the ORAD
b) INCREASED Force of Peristaltic Contractions of the CAUDAD Stomach
c) DECREASED Tone of the Pylorus
d) INCREASED Diameter and Inhibition of Segmenting Contractions of the Proximal Duodenum
**Gastric Emptying takes ~ 3 Hours!!!!
Gastric Emptying is closely regulated to provide adequate time for Neutralization of Gastric H+ in the Duodenum and sufficient time for Digestion and Absorption
- Regulation of Emptying results from the presence of Receptors that lie in the Small Intestine
Factors that INHIBIT Gastric Emptying:
a) RELAXATION of ORAD
b) DECREASED Force of Peristaltic Contractions
c) INCREASED Tone of Pyloric Sphincter
d) Segmentation Contractions in INTESTINE
Intestinal Mucosal Receptors Trigger Enterogastric Reflexes
- Information from the Duodenal Receptors to the Gastric Smooth Muscle is carried by Neurons of the SUBMUCOSAL and MYENTERIC PLEXUSES
- These receptors repost to the Physical Properties (Ex; Osmotic Pressure) and Chemical Composition (Ex: H+, Fat, and Protein) of the Intestinal Contents
- Receptor Activation TRIGGERS Neural and Hormonal responses that INHIBIT GASTRIC EMPTYING:
a) Fat and Protein induce the release of CCK, which in turn INCREASES GASTRIC DISTENSIBILITY
b) H+ Inhibitory effects are MEDIATED by INTRINSIC NEURAL REFLEX (ENS) involved Interneurons in the Myenteric Plexus
Effects of Peristaltic Contraction on Gastric Content
- There is no Gross Movement of Gastric Contents in-between Contractions!!!!
Slow Gastric Emptying is the most Common Problem associated with Disorders of Gastric Motility
SYMPTOMS:
- Fullness
- Loss of Appetitie
- Nausea
- Sometimes Vomiting
CAUSES:
- Gastric Ulcer (Scar Tissue)
- Cancer (Physical Obstruction)
- Eating Disorder (Anorexia Nervosa, Bulimia Nervosa, Obesity)
- Vagotomy (Was once used to Reduce Acid Secretion)
TREATMENT:
- Phyoroplasty
- Balloon Dilation
Gastroparesis
What is it?
- Slow emptying of Stomach/ Paralysis of Stomach
Who gets it?
- 20% Type I Diabetics (Some Type II)
Cause:
- High Blood Glucose damages VAGUS NERVE
- Idiopathic
- High Blood Glucose (Diabetic Gastroparesis)
Symptoms:
- Nausea, Vomiting, and early feeling of Fullness when Eating, Weight Loss, Abdominal Bloating, Abdominal Discomfort
Treatment:
- Goal is to Lower Blood Glucose
Large Particle of undigested residue remaining in the Stomach are emptied by Migrating Myoelectric Complexes (MMC)
- Migrating Myoelectric Complex = Migrating MOTOR Complex
- MMCs are PERIODIC, bursting Peristaltic contractions occurring during Fasting, in BOTH Stomach and Small Intestine
- MMCs occur at 90 Min INTERVALS
- MMCs are MEDIATED by MOTILIN!!!!!
- Feeding INHIBITS MMCs
- Absence of MMCs in the Stomach has been associated with GASTROPARESIS!!!!!!
Motility in the Small Intestine is Key for its Digestive and Absorptive Functions
Motility in the Small Bow Serve to:
- Mix the CYME with Digestive Enzyme and Pancreatic Secretions
- Expose Nutrients to the Intestinal Mucosa for Absorption
- Propel the UNABSORBED CHYME along the Small Intestine to the Large Intestine
There are TWO Types of Contractions:
1) SEGMENTATION CONTRACTIONS:
- Serve to Mix the Chyme and expose it to Pancreatic Enzyme and Secretions
2) PERISTALTIC CONTRACTIONS:
- Serve to Propel the Chyme toward the Large Intestine
Segmentation Contractions
- Generates Back and Forth Movements
- Produces NO FORWARD, Propulsive movement along the Small Intestine
Peristaltic Contractions
- BEHIND the BOLUS, CIRCULAR Muscle CONTRACTS and LONGITUDINAL Muscle RELAXES, where as in FRONT of the BOLUS, CIRCULAR Muscle RELAXES and LONGITUDINAL Muscle CONTRACTS
- Circular and Longitudinal Muscles work in OPPOSITION to Complement each other’s actions (Reciprocally innervated)
Contractions of the Intestine are Controlled by Activites of the ICCs and Smooth Muscle Cells, as well as Neural and Hormonal Responses
ELECTRICAL ACTIVITY:
ELECTRICAL ACTIVITY:
- Slow Wave Activity is ALWAYS PRESENT whether contractions are occurring or not
- Unlike in the Stomach, Slow Waves themselves DO NOT INITIATE Contractions in the Small Intestine
- Spike Potentials (AP) are NECESSARY for Muscle CONTRACTION to Occur
- Slow Wave Frequency sets the MAXIMUM FREQUENCY of CONTRACTIONS
Contractions of the Intestine are Controlled by Activites of the ICCs and Smooth Muscle Cells, as well as Neural and Hormonal Responses
ELECTRICAL ACTIVITY:
Cont!!!!
ELECTRICAL ACTIVITY:
- There is a Gradient in the MAXIMAL FREQUENCY of Contractions along the Small Intestine
- There is a Decrease in Frequency toward the ILEOCECAL JUNCTION
- Slow Wave Frequency Gradient:
a) Duodenum: 12 Cycles/ min
b) Jejunum: 10 Cycles/ min
c) Ileum: 8 Cycles/ min
Regulation of Peristaltic Contractions in the Small Intestine
- SEROTONIN (5-HT) is released by EECs and bonds to Receptors in Intrinsic Primary Afferent Neurons (IPANs), initiating the Peristaltic Reflex
- The MYENTERIC PLEXUS, located between the Longitudinal and Circular Smooth Muscle layers, mainly REGULATES the Relaxation and Contraction of the Intestinal Wall
- The SUBMUCOSAL (Meissner) Plexus senses the LUMEN Environment, among other Functions
Contractions of the Intestine are Controlled by activities of the ICCs and Smooth Muscle Cells, as well as Neural and Hormonal Responses
NEURAL INPUT:
- Peristaltic Reflex is mediated by the ENS
- In General, PNS STIMULATES and SNS INHIBITS CONTRACTIONS
HORMONAL INPUT:
- SEROTONIN, which is contained in large Quantities within the Small Bowel, STIMULATES CONTRACTIONS
- Certain PROSTAGLANDINS can STMULATE Contractions
- EPINEPHRINE, released from Adrenal Glands, INHIBITS Contractions
- GASTRIN, CCK, MOTILIN, and INSULIN Tend to Stimulate Contractions (Exact Role yet to be determined)
- SECRETIN and GLUCAGON tend to INHIBIT Contraptions (Exact Role yet to be determined)
Vomiting Reflex
- The MEDULLA Coordinates the VOMITING REFLEX
- Nerve impulses are transmitted by BOTH VAGAL and SYMPATHETIC AFFERENT Nerve Fibers to Multiple distributed NUCLEI in the Brain Stem
- The Vomiting Reflex involves REVERSE PERISTALSIS of the Small Bowel
ORDER OF EVENTS:
1) Reverse PERISTALSIS in the Small Intestine
2) RELAXATION of the Stomach and Pylorus
3) FORCED INSPIRATION to INCREASE Abdominal PRESSURE
4) Movement of the LARYNX
5) RELAXATION of the LES
6) CLOSURE of the GLOTTIS
7) FORCEFUL EXPULSION of GASTRIC CONTENTS
The Flow of Contents from the Small Intestine into the Large Intestine in partly regulated at the ILEOCECAL JUNCTION
- The ILEOCECAL SPHINCTER relaxes Periodically, during this time ILEAL CONTRACTIONS PROPEL Contents into the Large Intestine
- DISTENTION of the ILEUM causes RELAXATION of the SPHINCTER
a) ALLOWS flow of Contents from Ileum INTO the Colon - DISTENTION of the COLON causes CONTRACTION of the SPHINCTER
a) PREVENTS passage of Contents from the Colon to the Ileum
The Large Intestine’s Main Functions are Absorptive Water and Vitamins, and Conversion of Digested Food into Feces
LARGE INTESTINE:
- Cecum
- Ascending Colon
- Transverse Colon
- Descending Colon
- Sigmoid Colon
- Rectum
- Anal Canal
Anatomical Features of the Large Intestine
1) Muscle Layers arranged in Fibers
a) LONGITUDINAL
- Taenia Coli: 3 Flat bands of LONGITUDINAL Fibers that run from Cecum to Rectum
b) CIRCULAR
- Continuous for the Cecum to the Anal Canal
2) SPHINCTERS
a) Internal Anal Sphincter (SMOOTH MUSCLE)
b) External Anal Sphincter (SKELETAL MUSCLE)
3) HAUSTRAS:
- Small pouches that give the Large Intestine its Segmented Appearance
- Not fixed, Appear and Disappear
Innervation of the Large Intestine
1) ENS (Myenteric Pelxus)
- Concentrated Beneath TENAE
- Innervate Muscle Layers
2) PARASYMPATHETIC Nervous System
- VAGAL NERVE: CECUM, ASCENDING and TRANSVESE COLON
- PELVIC Nerves (Sacral Potion of the Spinal Cord, S2 to S4): DESCENDING and SIGMOID COLON, RECTUM
3) SYMPATHETIC Nervous System (T10- L2)
- Superior Mesenteric Ganglion: Proximal Regions
- Inferior Mesenteric Ganglion: Distal Regions
- Hypogastric Plexus: Distal Rectum and Anal Canal
- Somatic Pudendal Nerves: External Anal Sphincters
- *Major EXCITATORY Mediators: ACh and Substance P!!!!!
- **Major INHIBITORY Mediators: NO and VIP!!!!!
Motility in the Large Intestine is KEY for the Absorption of Water and Vitamins, and Conversion of Digested Food into Feces
- Segmentation Contractions
- Mass Movement
- Local Reflexes
- Defecation Reflex
- Defecation
SEGMENTATION CONTRACTIONS
- Occurs in the Cecum and Ascending Colon
- Appear, Disappear, and form again at another location within the Large Intestine
- At adjacent sites, contractions usually occur INDEPENDENTLY
- Cause LITTLE PROPULSION
- Serve to mix the contents of the Large Intestine
MASS MOVEMENTS
- Occur in the Colon, Over Large Distances, such as from the Transverse Colon to Sigmoid Colon
- Occur 1 to 3 times/day
- Move the content of the large Intestine over Long Distances and STIMULATE DEFECATION REFLEX
- A FINAL Mass Movement propels the Fecal Content into the Rectum
Poor Motility vs Excess Motility
- POOR MOTILITY causes GREATER ABSORPTION, and HARD FECES in Transverse Colon cause CONSTIPATION
- EXCESS MOTILITY causes LESS ABSORPTION and DIARRHEA or Loose Feces
Motility of the Rectum and Anal Canal
- Rectum is usually EMPTY
- FREQUENCY of SEGMENTATION CONTRACTIONS in the Rectum’s Upper Region > Sigmoidal Colon
- Rectum fills INTERMITTENTLY
a) Mass Movements
b) Segmentation Contractions - As it fills with Feces, Smooth Muscle wall of the Rectum CONTRACTS and Internal Anal Sphincter RELAXES (RECTOSPHINCTERIC REFLEX)!!!!!!!!!!
- The External Anal Sphincter is TONICALLY CLOSED (Under Voluntary Control)
- Urge to Defecate occurs when the RECTUM FILLS 25% of its CAPACITY
Defecation reflex and the Act of Defecation
- The RECTOSPHINTERIC REFLEX and the act of Defecation are under Neural Control
a) Part of the Control lies in the ENS
b) The Reflex is reinforced by the ACTIVITY of Neurons within the Spinal Cord - The Sensation of RECTAL DISTENTION, as well as the VOLUNTARY CONTROL of the External Anal Sphincter, is mediated by Pathways WITHIN the Spinal Cord that lead to the CEREBRAL CORTEX
- Destruction of these Pathways causes a LOSS of Voluntary Control of Defecation
***In PARAPLEGIC PATEINTS lacking TONIC CONTRACTION of the External Anal Sphincter, the RECTOSPHINCTERIC REFLEX results in DEFECATION
Defecation Reflex and the Act of Defecation Cont
- Defecation is PREVENTED by the External Anal Sphincter
- If the Rectosphincteric Reflex is elicited at a time when Evacuation is Convenient, DEFECATION OCCURS
- Defecation is accomplished by a Series of Voluntary and Involuntary Acts
Hirschspring Diseasae
CAUSE:
- Ganglion Cells ABSENT from Segment of Colon
RESULT:
- VIP Levels Low —> Smooth Muscle Constriction
- Loss of Coordinated Movement —> Colon Contents accumulate (Colon Equivalent of Achalasia)
TREATMENT:
- Surgical resection of Colon Segment lacking Ganglia
- Present at Birth, it causes DIFFICULTY PASSING STOOL
- The MAIN SYMPTOM is a Newborn’s FAILURE TO HAVE A BOWEL MOVEMENT WITHIN 48 HOURS AFTER BIRTH!!!!!!!!
- Failure to PASS MECONIUM Shortly after Birth
- Other Symptoms on Newborn/ Infant Include: Poor Feeding, Jaundice, and Vomiting
- In older Children symptoms include: Constipation, Swollen Belly, Malnutrition
Diverticulitis
- Diverticula (Diverticulum Singular) are SMALL SACS of Intestinal Lining that BULGE OUTWARD at Weak Spots
- Caused by EXCESS PRESSURE in the Colon that causes WEAK SPOTS in Colon to Bulge OUT and become Diverticula
- Increases with Age (10% > 40, 50% > 60, ~100% > 80)
TREATMENT:
- Dietary and Lifestyle Interventions
Primary Peristaltic Wave CANNOT occur Without the Vagus, Secondary Peristaltic Waves CAN
- Pharynx and Upper Part of the Esophagus consist of STRIATED MUSCLE Innervated by the Vagus and Glossopharyngeal Nerves
- Mid and lower Esophagus consist of Smooth Muscle, and are Strongly controlled by VEGUS NERVES that act through the MYENTERIC Nervous System
- If VAGUS Nerve is cut, MYENTERIC PLEXUS become Excitable enough after Several days to cause STRONG SECONDARY PERISTALTIC WAVES!!!!!!!!!!!!
Summary of the Entero-Gastric Reflex
- Negative Feedback from Duodenum will SLOW DOWN the Rate of Gastric Emptying
Multiple Mechanisms are Involved:
1) Acid in Duodenum —> Stimulate SECRETIN Release —> Inhibit Stomach motility via GASTRIN INHIBITION
2) FATS in Duodenum —> Stiulate CCK and GIP —> Inhibit Stomach Motility
3) HYPERTONICITY in Duodenum —> (Unknown Hormone) —-> Inhibit Gastric Emptying
Summary fo Reflexes
1) VAGO-VAGAL REFLEX (Long Reflex):
- Generally Stimulatory
- Increases Motility, Secretomotor, Vasodilatory Activities
- Vagus carries both Afferents (75%) and Efferents (25%)
2) INTESTINO-INTESTINAL REFLEX (Short Reflex):
- Generally Inhibitory
- Involving ONLY the ENS and COMPLETELY INDEPENDENT of the ANS (Atropine has no Effect on it!)
- Ex: Ileocecal Sphincter (SM) acts by Intestine-Intestinal Reflexes
3) ENTEROGASTRIC REFLEX :
- Negative Feedback from Duodenum, will Slow down the rate of Gastric Emptying
4) GASTROILEAL REFLEX (GASTROENTERIC):
- Gastric distension relaxes Ileocecal Sphincter
5) GASTRO and DUODENO-COLIC REFLEXES:
- Distention of Stomach/ Duodenum initiates MASS MOVEMENTS
6) DEFECATION REFLEX (Rectosphincteric):
- Rectal Distention intimates Defecation
Diverticular Disease/ Diverticulitis
- Diverticula (Diverticulum Singular) are SMALL SACS of Intestinal Lignin that BULGE OUTWARD at WEAK SPOTS
- Caused by EXCESS PRESSURE in the Colon that causes WEAK SPOTS in Colon to bulge out and become Diverticula
- Diverticula can occur anywhere in the Colon, but most commonly near the end of the Colon on the LEFT SIDE
- When a patient has Diverticula in the Colon this is called DIVERTICULOSIS, or DIVERTICULAR DISEASE
- If a Diverticulum becomes infected and the area around the Diverticulum is Swollen, it is called DIVERTICULITIS
- 10 to 25% of patients with Diverticular Disease will Experience it
Contractions of the Muscular Propria Mix and Circulate the Content of the Lumen and Propel it through the GI Tract
FUNCTIONAL LAYERS:
1) Mucosal Layer:
- MUSCULARIS MUCOSA: Consists of SM, its Contractions Change the Shape and Surface area of the Epithelium
2) Submucosa
3) Muscle Layer (Muscular Propria)
- SM layers, PROVIDE MOTILITY to the GI Tract
a) Circular Muscle
b) Longitudinal Muscle
4) Serosa
The Myenteric Plexus Controls mainly the Gastrointestinal Movements
ENS:
1) SUBMUCOSAL PLEXUS
- In the Submucosa
- Mainly controls GI Secretions and Local Blood Flow
2) MYENTERIC PLEXUS (AUERBACH’S)
- Between the Longitudinal and Circular Layers
- Mainly Controls GI Movements
**PACEMAKER regions in the Myenteric and Submucosal Plexuses GENERATE SPONTANEOUS SLOW WAVE ACTIVITY!!!!!!!
Primary Peristaltic Wave CANNOT Occur without the Vagus, Secondary peristaltic Waves CAN
- Pharynx and Upper part of the Esophagus consist of STRIATED MUSCLE innervated by the VAGUS and GLOSSOPHARYNGEAL NERVES
- Middle and Lower Esophagus consist of SM, and are Strongly controlled by VAGUS NERVES that ACT through the MYENTERIC Nervous System
*****If the VAGUS Nerve is Cut, MYENTERIC PLEXUS becomes excitable enough after SEVERAL SAYS to cause STRONG SECONDARY PERISTALTIC WAVES!!!!!!!!!
Summary of Entero-Gastric Reflex
- NEGATIVE Feedback from Duodenum will SLOW DOWN the RATE of Gastric Emptying
Multiple Mechanisms involved:
1) ACID is DUODENUM —-> Stimulate SECRETIN Release —> INHIBIT STOMACH Motility via Gastrin Inhibition
2) FATS in Duodenum —> Stimulate CCK and GIP —–> INHIBIT Stomach Motility
3) Hypertonicity in Duodenum —-> (Unknown Hormone) —–> INHIBIT Gastric Emptying
What Clinical Signs help confirm Diverticulitis
- Constipation
- Flatus
- Left Sided Abdominal Pain
- Tenderness
- Fever
- Tachycardia
