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GIGU Exam 1 > Motility In The GI System > Flashcards

Motility In The GI System Flashcards

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1
Q

Muscularis Mucosae

A

SM that contract to change the shape and SA of the epithelium

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2
Q

Slow waves are found where
What is it
when do APs occur

A

In the SM of GI tract
Depolarization and repolarization make no AP
AP happens when depolarization moves above threshold and = mechanical response (due to H. Or Nerve)
* slow waves sets the f of APs

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3
Q

Phasing contractions and where are they found

A

Periodic contractions followed by relaxation

Upper esophagus, Antrum stomach, SI, anything for mixing and propulsion

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4
Q

Tonic Contractions and where are they found

A

Constant level of contraction without regular relaxation periods
Lower esophagus, Orad stomach, Ileocecal sphincter, internal anal sphincter

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5
Q

How to increase the contraction strength

A

Higher number of AP on top of the slow wave

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6
Q

What increases AP on slow waves

A

ACH, Stretch, and Parasympathetics increase Amplitude and number of APs(strength of contraction)

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7
Q

what decreases APs of slow waves

A

NE and Sympathetics decrease number of APs(strength of contractions)

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8
Q

Submucosal plexus (meissner’s)

A

In the submucosa externally to it

GI secretions and local BF

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9
Q

Myenteric Plexus (Auerbach’s)

A

GI movements

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10
Q

The submucosa and myenteric plexus are part of the

A

ENT which does not need the CNS to operate

However it can in some instances relay information to the CNS

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11
Q

Interstitial cells of Cajal (ICC)

A

Pacemaker cells in the GI SM
They initiate and generate SLOW WAVES (spontaneous slow waves in ICC spreads to nearby SM cells by gap junctions)
The control strength of contraction

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12
Q

Spontaneous SLOW WAVES in the ICC due to

A

Opening of voltage gated CA+2 channels, pass along through gap unctions to open Ca+2 channels of SM cells

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13
Q

Mastication

A

Voluntary and in voluntary controlled by CN5 with nuclei in brain stem (Mastication Reflex)

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14
Q

4 phases of swallowing

A

1 . Oral phase : Voluntary - initiate swallowing

  1. Pharyngeal phase : Involuntary - soft plate pulled UP = epiglottis moves = UES relaxes = peristaltic wave of contractions initiated by pharynx ——> food moves to UES
  2. Esophageal Phase : Involuntary- ENS and swallowing reflex controls this, = Primary and secondary peristaltic waves to move food past LES (continuous from pharynx wave)
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15
Q

How the pharynx starts the peristaltic wave of contraction

A
  1. Food is sensed in pharynx by CN X + CN 9
  2. CN X + CN 9 go to the swallowing center (medulla)
  3. Sends info to brain stem nuclei
  4. Send signal through the nucleus ambiguous to pharynx to contract
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16
Q

Primary Peristaltic wave in the epiglottis

A

Continuous with pharyngeal wave contraction
Controlled by medulla also
Uses CN 10 to send signal from here
NONE after VAGOTOMY

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17
Q

Secondary Peristaltic wave

A

Occurs if primary doesn’t get rid of all food or during gastric reflex
Controlled by Medulla (CN X ) and ENS
Not continuous or so trolled by any previous peristaltic wave contraction = UES does not need to open
CAN HAPPEN STILL AFTER VAGOTOMY

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18
Q

How is the pressure at rest through the esophagus

A

Upper part (UES) : high pressure due to no acid reflux, above 0mmHg
A little lower (level of Thorax) : below 0mmHg - flaccid
Right below or at diaphragm: a little above 0mmHg,
LES : HIGH pressure above 0mmHg
Fundus of stomach : HIGH above 0mmHg

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19
Q

How is the pressure during swallowing through the esophagus

A

Upper (UES) : decreases quick to open
(Level of thorax) : increase after the initial UES opening
At or below diaphragm: slight increase spike
LES : broad decrease spike (starts even before food is right there)
Fundus : very slow broad decrease (starts before food comes there)

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20
Q

Reason UES and LES are closed at all times unless food is passing

A

To keep air out of esophagus at upper end

To prevent gastric acid contents out from lower end

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21
Q

What happens in achalasia

A
  1. The peristaltic waves impaired
  2. LES doesn’t relax all the way (when swallowing)
  3. LES resting pressure is very elevated
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22
Q

Reasons for achalasia to occur

A

Ganglionic cells in the myenteric plexus (in Muscularis Externa) decreased
= inhibitor neurons make NO + VIP —> damaged specifically
= no contraction or relaxation when needed

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23
Q

Achalasia Sx:

A

Regurgitation of food liquid and solid
Hard swallow (DYSPHAGIA)
Heartburn
Chest pain

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24
Q

What happens in GERD

A

Barrier between esophagus and stomach changes due to weakened LES (abnormally relaxed)
= gastric reflux is common (during pregnancy, lifting, large meal)—> they tend to relax LES
= gastric acid + bile + pepsin into esophagus—> heartburn and regurgitation of acid

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25
What can make GERD happen and complications
Persistent reflux and inflammation damages the ENT neurons in the myenteric plexus that signal contraction GI bleeding, (irritation) Esophagitis, Barrett’s esophagus, scarring in esophagus
26
CASE 1: 5 years Dysphagia. HTN. Foods stick to upper sternum area after meal. Can get it down with repeated swallows or drinkin water. Spontaneous regurgitation and cough at night. Weight loss Chest pain, no heartburn, traveled to mexico one month before.
DX: Achalasia | Chagas Disease
27
Innervation of the stomach
Extrinsic innervation - para and sympa | Intrinsic innervation - myenteric and submucosa plexus
28
to pass food rom orad to the caudal is
Receptive relaxation Decrease P and Increase V in orad region VAGOVAGAL REFLEX
29
Orad function
Little contraction and mixing, more for receiving food
30
CCK in the duodenum causes
Decrease contraction Increase Gastric Distensibility * in stomach
31
Contraction strength and velocity in stomach
Increases as you move closer to the Pyloris (from mid stomach)
32
REPULSION
When increased P on Pyloris closes it and food is pushed back up to the Orad to mix food more
33
How long food goes to duodenum completely
3-4hrs
34
What increases AP and contraction force in stomach
PARASYMPATHETIC (*CN10), GASTRIN, MOTILIN
35
What decreases AP and contraction force in stomach
SYMPATHETIC, SECRETIN, GIP
36
4 factors promoting gastric emptying to the duodenum
1. Decrease DISTENTION of orad(contract more) 2. Decrease TONE of Pyloris (Relax more) 3. Increase FORCE of Perictaltic contractions of Caudal stomach 4. Increase DIAMETER and INHIBIT contraction of proximal duodenum
37
3 factors that inhibit gastric emptying
1. Relax orad 2. Decrease force of peristaltic contraction of caudal stomach 3. Increase pyloric tone and proximal duodenum contractions
38
Entero-Gastric Reflex in duodenum is ACID FATS HYPERTONIC
When contractions are high in duodenum = - feedback to stomach to not empty, using secretin, GIP, CCK (To keep pH right and not overwhelm duodenum) 1. Acid = secretin ——I stomach (by —I Gastrin) 2. Fats + AA = CCK + GIP —— I stomach 3. Hypertonicity = unknown H. ——I Gastric emptying
39
Gastric emptying disorder Sx: Causes Tx:
Sx: fullness, Loss of appetite, N, V Causes: Gastric ulcer, cancer, eating disorder, vagotomy (used in past to reduce acid secretion) Tx: pyloroplasty, balloon dilation
40
Gastroparesis
Slow emptying of stomach or paralysis of stomach Common cause = diabetes (20% T1D) Vagus N injury (no mechanical obstruction) Sx: N, V, fullness, weight loss, boating ,ABD discomfort
41
How are large particles of undigested and bacteria that remain in the stomach
MMC (Migrating Myoelectric Complex, Migrating Motor Comlex) ONLY DURING FASTING Periodic bursting peristaltic contractions moving from the fundus of stomach to the rectum (90min) to clean the GI MOTILIN = important role
42
Disfunctioning MMC
``` Bacterial overgrowth (SIBO) - if in SI = can cause motility dysfunction in SI —> N, anorexia, bloating ```
43
How is SI digestion happening | 2 types of contraction
1. Segmentation contractions = Compress in middle of food boules and makes it split, relaxes and 2 halves come back together No forward movement, allows enzymes to mix and absorb 2. Peristaltic Contraction = circular and longitudinal muscles move food forward Orad——> Caudal
44
How do circular and longitudinal muscles work together
When one contracts the other relaxes (always opposite) to move the food
45
What electrical impulses are present in the SI
SLOW WAVES ; always present even with no contractions ——> they DONT initiate contractions (the AP is what initiate any contraction) ——> they do set the number of contractions/min by increasing frequency
46
SLOW WAVE f in the SI
Highest at proximal SI | Decreases down the SI
47
How signals in lumen are collected and make a GI response
Wall of SI : cells sense mechanical/contents in lumen (enterochromaffin cells) ——> SEROTONIN ——> IPAN receptor ——> interneurons (excitatory + inhibitor)——> muscle for peristaltic reflex *there are interneurons (ACH + Substance P - excitatory) and (VIP + NO- inhibitory) that get info from enterochromaffin
48
``` Para and sympa Serotonin Prostaglandin Epinephrine Gastrin CCK Motilin Insulin Secretin Glucagon ```
``` Para = stimulates contraction Sympa = inhibits contraction ``` ``` Serotonin = stimulates contraction Prostaglandin = stimulates contraction Epinephrine = inhibits contractions Gastrin = increase contractions CCK = increase contractions Motilin = increase contractions Insulin = increase contractions Secretin = inhibit contractions Glucagon = inhibit contractions ```
49
What coordinates vomiting reflex
Uses Medulla which uses VAGUS + SYMPATHETIC AFFERENTS to many places in the Brianstem ——> chemoreceptor zone by area postrema——> Medulla——> vomit reflex 1. Revers peristaltic contractions 2. Stomach relaxed 3. Inspire forcibly to increase ABD P 4. LES relaxations + Close glottis 5. Movement of larynx
50
Ileocecal Junction | When is sphincter relaxed/ contracted
``` Relaxed = when ileum is distended Contracted = when colon is dilated ```
51
What do the Longitudinal Muscles of the LI have
Taeniae Coli = 3 bands from cecum to rectum
52
Circular muscles of LI
Cecum to Anal canal | HAUSTRA are formed , disappear and reappear
53
Pelvic Splanchnic N innervates
Inner Anal Sphincter (parasympathetic)
54
Peudendal N innervates
External Anal Sphincter (somatic)
55
ENT (myenteric) innervates
under teneae coli, and muscles layer of external Muscularis
56
Parasympathetic NS innervates in LI
Vagus ——> Cecum, A.C, T.C. | Pelvic NS S1-S4 ——> D.C, S.C, Rectum
57
Sympathetic innervates in LI
Superior mesenteric——> Proximal regions Inferior Mesenteric ——-> Distal Regions Hypogastric——> Distal Rectum and Anal Canal
58
Unique feature of LI to make poop
MASS MOVEMENT 1-3 times a day Defacation reflex In colon (T.C is most common) over large distance
59
LI absorption
VIT and H2O
60
Rectum movement
Mass movement Segmented contractions 1. SM contract + Internal anal sphincter relaxes *RETROSPHINTERIC REFLEX) 2. External Anal sphincter closes when you want to and don’t want to poop at the moment
61
What controls the RECTOSPHINCTERIC REFLEX
Neural ENS and spinal cord nerves(senses rectal distension) ——> muscles External sphincter nerves travel to cerebral cortex ——> muscle * if damaged = problems of voluntary control of poop
62
Normal tone means
Muscle or sphincter in not defected | If there is a problem it is the nerve in this case
63
Hirschsprung Disease
Ganglion cells absent from colon (VIP levels are low) = SM contractions + no controlled movement = feces accumulate = if at birth : congenital megacolon (no meconium), jaundice, X feeding =older patients : constipation, malnutrition =Tx: surgery to put ganglia from other locations to the part of colon without

GIGU Exam 1 (19 decks)

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