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GIGU Exam 1 > Motility In The GI System > Flashcards

Motility In The GI System Flashcards

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
Q

What can make GERD happen and complications

A

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

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26
Q

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.

A

DX: Achalasia

Chagas Disease

27
Q

Innervation of the stomach

A

Extrinsic innervation - para and sympa

Intrinsic innervation - myenteric and submucosa plexus

28
Q

to pass food rom orad to the caudal is

A

Receptive relaxation
Decrease P and Increase V in orad region
VAGOVAGAL REFLEX

29
Q

Orad function

A

Little contraction and mixing, more for receiving food

30
Q

CCK in the duodenum causes

A

Decrease contraction
Increase Gastric Distensibility
* in stomach

31
Q

Contraction strength and velocity in stomach

A

Increases as you move closer to the Pyloris (from mid stomach)

32
Q

REPULSION

A

When increased P on Pyloris closes it and food is pushed back up to the Orad to mix food more

33
Q

How long food goes to duodenum completely

A

3-4hrs

34
Q

What increases AP and contraction force in stomach

A

PARASYMPATHETIC (*CN10), GASTRIN, MOTILIN

35
Q

What decreases AP and contraction force in stomach

A

SYMPATHETIC, SECRETIN, GIP

36
Q

4 factors promoting gastric emptying to the duodenum

A
  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
Q

3 factors that inhibit gastric emptying

A
  1. Relax orad
  2. Decrease force of peristaltic contraction of caudal stomach
  3. Increase pyloric tone and proximal duodenum contractions
38
Q

Entero-Gastric Reflex
in duodenum is ACID
FATS
HYPERTONIC

A

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
Q

Gastric emptying disorder
Sx:
Causes
Tx:

A

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
Q

Gastroparesis

A

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
Q

How are large particles of undigested and bacteria that remain in the stomach

A

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
Q

Disfunctioning MMC

A 
Bacterial overgrowth (SIBO) - if in SI
= can cause motility dysfunction in SI —> N, anorexia, bloating
43
Q

How is SI digestion happening

2 types of contraction

A
  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
Q

How do circular and longitudinal muscles work together

A

When one contracts the other relaxes (always opposite) to move the food

45
Q

What electrical impulses are present in the SI

A

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
Q

SLOW WAVE f in the SI

A

Highest at proximal SI

Decreases down the SI

47
Q

How signals in lumen are collected and make a GI response

A

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
Q 
Para and sympa 
Serotonin 
Prostaglandin 
Epinephrine 
Gastrin
CCK
Motilin
Insulin
Secretin
Glucagon
A 
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
Q

What coordinates vomiting reflex

A

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
Q

Ileocecal Junction

When is sphincter relaxed/ contracted

A 
Relaxed = when ileum is distended
Contracted = when colon is dilated
51
Q

What do the Longitudinal Muscles of the LI have

A

Taeniae Coli = 3 bands from cecum to rectum

52
Q

Circular muscles of LI

A

Cecum to Anal canal

HAUSTRA are formed , disappear and reappear

53
Q

Pelvic Splanchnic N innervates

A

Inner Anal Sphincter (parasympathetic)

54
Q

Peudendal N innervates

A

External Anal Sphincter (somatic)

55
Q

ENT (myenteric) innervates

A

under teneae coli, and muscles layer of external Muscularis

56
Q

Parasympathetic NS innervates in LI

A

Vagus ——> Cecum, A.C, T.C.

Pelvic NS S1-S4 ——> D.C, S.C, Rectum

57
Q

Sympathetic innervates in LI

A

Superior mesenteric——> Proximal regions
Inferior Mesenteric ——-> Distal Regions
Hypogastric——> Distal Rectum and Anal Canal

58
Q

Unique feature of LI to make poop

A

MASS MOVEMENT
1-3 times a day
Defacation reflex
In colon (T.C is most common) over large distance

59
Q

LI absorption

A

VIT and H2O

60
Q

Rectum movement

A

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
Q

What controls the RECTOSPHINCTERIC REFLEX

A

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
Q

Normal tone means

A

Muscle or sphincter in not defected

If there is a problem it is the nerve in this case

63
Q

Hirschsprung Disease

A

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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