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Gastroenterology I > Motility Physiology > Flashcards

Motility Physiology Flashcards

1
Q

circular vs longitudinal muscle, what does each do with contraction?

A

circular = lowers diameter of segment

long = lowers length of the segment.

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2
Q

what happens in the GI that is a unique feature

A

slow waves done by the smooth muscle!!! they are NOT AP’s!

the membrane potential goes up and down by the cells of cajal. as it gets higher, it is easier for APs to happen, thus the slow waves are determining the contraction.

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3
Q

When does tension happen?

A

slow waves influence contraction, and tension is contraction which happens after the action potentials.

essentially mechanical response follows the electrical response?

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4
Q

how do you increase contraction of the GI?

A

neural and hormonal activity.

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5
Q

What’s the difference between phasic and tonic contractions? examples?

A

Tonic contraction = constant level of contraction without regular periods of relaxation (e.g. spinchters)

phasic = periodic cont reactions followed by relaxation (pretty much everywhere)

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6
Q

Greater APs means what? How does this happen?

what does the opposite of this?

A

larger contractions

so if the slow wave is more + there would be more APs. This is done by ACh, which increases amplitude of slow waves.

NE, which decreases the amplitude of slow waves.

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7
Q

What stimulates slow waves and APs

hyper polarization of slow waves?

A

stretch, acetylcholine, PNS

NE, sympathetics

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8
Q

What are the pacemaker regions in the enteric nervous system? why does this work?

A

myenteric plexus + submucosal plexus

doesn’t need the CNS to generate slow wave activity.

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9
Q

What are the two parts of the ENS and what does it control?

A

submucosal plexus –> mainly controls GI secretions and local blood flow

myenteric plexus (Auerbach) –> controls GI movements

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10
Q

Where are the slow waves generated?

A

Interstitial cells of Cajal –> generate the slow wave

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11
Q

What do Interstitial cells of Cajal do?

A

generate the slow waves and pass conduction to smooth muscle via gap junctions

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12
Q

What is mastication?

what innervates it?

voluntary or involuntary?

what is it controlled by?

A

chewing the food and prepping it to go onto the esophagus.

5th cranial nerve (trigeminal)

It’s voluntary and involuntary (chewing reflex)

nuclei in the brain stem

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13
Q

What are the three phases of swallowing?

A 
Oral phase (voluntary)
Pharyngeal phase (involuntary)
Esophageal phase (involuntary)
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14
Q

From the pharynx to the LES, what is the esophagus composed of?

A

from the pharynx to the esophagus (after the UES), it’s voluntary so striated muscle.

below that is smooth muscle

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15
Q

which is longer, pharyngeal or esophageal?

A

esophageal

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16
Q

The involuntary swallowing reflex is controlled by what?

pathway?

A

the medulla

food in pharynx -> afferent sensory input via vagus –> swallowing center (medulla) –> brainstem nuclei –> efferent input to the pharynx

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17
Q

What are the two peristaltic waves? where are these present??

A

esophagus!

primary = controlled by the medulla, continuation of pharyngeal peristalsis. Vagotomy destroys this.

secondary: occurs if primary wave fails to empty the esophagus or if gastric contents reflux. occurs even after a vagotomy (doesn’t rely on the vagus like primary)

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18
Q

Why is there a drop in pressure at the UES at first and then it goes super high?

A

it relaxes and then the bolus goes through and it needs to close really quickly so that’s why it goes back up really fast.

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19
Q

What’s important to note about the LES and Fundus during the swallowing reflex?

A

they both relax before the bolus even gets there.

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20
Q

Why is the intrathoracic location of the esophagus a challenge?

how is it solved?

A

we need to keep air out of the esophagus at the upper end and the lower end needs to keep gastric juice out.

UES and LES are always closed unless bolus is passing.

21
Q

Achalasia?

A

impaired peristalsis, incomplete LES relaxation during swallowing, so elevated LES resting pressure.

so food gets stuck because the enteric nervous system is not good. back flow of food, chest pain, dysphagia.

22
Q

What is GERD?

A

LES is relaxing more than it should. contents come up to the esophagus. if chronic it’s. Barrett’s esophagus.

happens because of motor abnormalities that result in abnormally low pressure of the LES.

23
Q

What tests do you do for achalasia to check?

A

barium swallow test and esophageal motility studies (manometry)

24
Q

What is receptive relaxation? what part of the stomach is doing this?

what hormone lowers contractions and increases gastric distensibility of this?

A

Orad… lower pressure and higher volume of the road region (vasovagal reflex!)

the orad exhibits little contractile activity.

CCK

25
Q

What happens in the caudal region of the stomach?

what’s the max frequency of slow waves of the stomach?

A

the farther you get into the stomach, the more intense the peristaltic wave is. they increase in force and velocity as they approach the pylorus.

3-5/min

26
Q

What happens at the antrum as the peristaltic wave moves from mid stomach to antrum?

A

the wave of contraction also hits the pyloric sphincter which closes, meaning the bolus is chopped up and some of it doesn’t make it to the duodenum. in this case then it’ll retropulse backwards and be mixed again and grounded to smaller bits.

27
Q

What does parasympathetics do to contractions? what other enzymes do this too?

same thing for SNS

A

increase AP and force of contraction… also gastrin (secretion of acid) and motilin

decrease AP and force of contraction… also secretin and GIP

28
Q

what is GIP?

A

gastrin inhibitory peptide

29
Q

What increases the rate of gastric emptying?

A

lower distensibility, so the less it’s able to be stretched or enlarged. it’s at it’s breaking point pretty much. (constricted orad)

higher force of contraction of caudal stomach

relaxed pylorus (tone)

higher diameter and inhibition of segmenting contractions of the proximal duodenum

30
Q

What lowers the rate of gastric emptying?

A

higher distensibility (relaxation of orad)

lower force of contraction

higher ton of pylorus

enterogastric reflex

31
Q

What is the entero-gastric reflex?

what are some triggers?

A

negative feedback from the duodenum will slow down the rate of gastric emptying.

high acid, high fats, high tone of the duodenum

acid –> stimulates secretin release –> inhibits stomach motility via gastrin inhibition’s

fats –> stimulate CCK and GIP –> inhibits

32
Q

What’s the most common problem with disorders of motility?

A

slow gastric emptying.

33
Q

what is Gastroparesis

A

paralysis of the stomach in the absence of mechanical obstruction.

Diabetes mellitus is common cause.

34
Q

What is the MMC?

when is it active?

A

migrating myoelectric complex

any large particle of undigested residue remaining in the stomach are emptied by this.

it’s active when we’re fasting… inhibited during the feeding.

it sweeps from the stomach all the way down to the colon.

occur at 90 min intervals.

35
Q

what plays a significant role in MMC?

A

motilin

36
Q

What are the main motility patterns of the small intestine?

A

segmentation contractions (generates back and forth movements to mix. IT HAS NOTHING TO DO WITH PROPELLING FORWARD

peristaltic contractions –> circular and longitudinal muscles work in opposition!

one is relaxing, one is contracting in order to propel it forward.

37
Q

what’s the difference between the stomach and small intestine for the slow waves?

A

slow waves themselves do not initiate contractions in the small intestines. you NEED action potentials for muscle contraction to occur.

38
Q

duodenum vs jejunum vs ileum cycles/min?

A

12, 10, 8

39
Q

What do IPANs do?

what binds to the IPAN that starts the peristaltic reflex?

what is the overall regulator though?

A

they’re intrinsic primary afferent neurons

they’re relaying information from the wall or whatever (pressure, etc), and either telling interneurons to do stuff via an excitatory motor neuron or inhibitory motor neuron

Serotonin that’s released by enterochromaffin cells

myenteric nervous system.

40
Q

ACH, VIP, NO, Substance P, which ones are excitatory for contraction, which are for relaxation?

A

ACH and Substance P for contraction

41
Q

Serotonin, prostaglandins, Epinephrine, gastrin, CCK, motion, insulin, secretin, glucagon

which ones inhibit contractions?

A

epinephrine, secretin, glucagon

42
Q

Explain the vomiting reflex

A

coordinated by the medulla

nerves are transmitted from the vagus or the sympathetic afferents.

reverse peristalsis in the small intestine, the stomach and pylorus relaxes, there is forced inspiration, movement of larynx, LES relaxation.

43
Q

How many longitudinal muscles are there in the large intestine?

A

3 flat bands of taeniae coli.

44
Q

What nerve innervates the external anal sphincter?

internal?

A

somatic Pudendal N.

pelvic splanchnic N

45
Q

What sympathetic nervous system nerves innervate the large intestine?

A

superior mesenteric ganglion (proximal regions)
inferior mesenteric ganglion (distal regions)

hypogastric plexus (distal rectum and anal canal)

46
Q

What is the motility in the large intestine?

A

mass movement. 1-3 times per day.

stimulate defecation reflex. it propels the fecal content into the rectum.

47
Q

what is the key of the large intestine for what it does?

A

motility is needed for absorption of water and vitamins and conversion of digested food into feces.

from the beginning of the large intestine is watery, middle is mush, end is solid

48
Q

what happens for the internal sphincter and external sphincter during pooping?

A

internal sphincter relaxes, and walls of rectum contracts (rectosphincteric reflex), but you can hold it because of the external anal sphincter being under voluntary control.

49
Q

Hirschsprung is what?

A

ganglion cells absent from segment of colon.

Gastroenterology I (5 decks)

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