Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Physiology Exam 5 > 59 - GI Gastric Motility > Flashcards

59 - GI Gastric Motility Flashcards

1
Q

What are the three basic mechanical movements of the stomach?

A

1 - Storing
2 - Churning
3 - Emptying

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is gastric storing?

A

Stomach fills and stores contents

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is gastric churning?

A

Mixing and initiating digestion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is gastric emptying?

A

Food delivery to the duodenum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the two steps to gastric storing?

A

1 - Receptive relaxation

2 - Gastric accommodation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Describe receptive relaxation

A
  • A vagovagal reflex that is initiated by swallowing
  • Includes the relaxation of the stomach in anticipation of food
  • The LES and proximal stomach relax
  • The goal of receptive relaxation is to have a rise in gastric volume without a rise in gastric pressure
  • There is NO cholinergic or adrenergic hormone signaling here
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Describe gastric accommodation

A
  • Stomach relaxes in response to gastric filling - DISTENSION is the key stimulus
  • Distention is sensed by mechanoreceptors
  • The result is NO release which relaxes smooth muscle
  • This causes the fundus of the stomach to dilate
  • This is primarily regulated by the ENS, but modulated by the vagus nerve
  • Again the goal here is to have a rise in gastric volume without a rise in pressure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the three types of gastric churning that occurs?

A

1 - Propulsion
2 - Retropulsion
3 - Grinding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Describe propulsion

A
  • Movement of contents toward the antrum/pylorus region
  • Initiated by pacemaker cells near the greater curvature of the stomach
  • Note that the pylorus is still closed at this point
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Describe retropulsion

A
  • Pulverization and shearing of food particles
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Describe grinding

A
  • Food is trapped in antrum
  • Products that are smaller than 2 mm pass through the pylorus
  • Particles that are larger than 2 mm will eventually pass into duodenum during the interdigestive period (2 hours later)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Describe factors that control the rate of gastric emptying

A

Rate of emptying

  • Rate of gastric emptying depends upon the content of the ingested material
  • Protein and lipids slow things down
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How is gastric emptying controlled?

A

Neuronal and hormonal regulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What three hormones control gastric emptying?

A
  • Secretin
  • CCK
  • Gastrin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What four neurotransmitters control gastric emptying?

A
  • ACh
  • NO
  • 5-HT
  • VIP
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the function of CCK?

A

CCK: promote digestion of food in the duodenum while limiting throwing more food (from the stomach) into the mix

CCK responds to fat – gallbladder is going to contract because it contains bile – which emulsifies fats

Cholicystokinin
As fat enters the duodenum, it stimulates the release of CCK
This feeds back and delays gastric emptying
The more fat you eat in a meal, the more CCK that is release, the more the meal will remain in the stomach to allow for adequate breakdown
This allows them to have a high surface area to be broken down more

17
Q

What is the function of secretin?

A

Released in response to high HCl in stomach

Protective in function

18
Q

Role of CCK and gastrin

A

CCK and gastrin are similar in that they impair gastric emptying to break down fat or protein, respectively, to the smallest possible form – this means more efficient digestion as smaller particles diffuse faster

19
Q

Role of NO and VIP

A

NO and VIP are the “gate-keepers” of the pyloric sphincter

20
Q

What is emesis?

A

Vomiting

- Expulsion of gastric and duodenal contents from the GI tract via the mouth

21
Q

What is emesis preceded by?

A
  • Nausea
  • Tachycardia
  • Dizziness
  • Sweating
  • Mydriasis
  • Retching
  • Increased saliva production
22
Q

Describe the series of events of vomiting

A
  • Irritation of GI mucosa
  • Afferent fibers are activated
  • The vomiting center of the brain is activated
  • This triggers a wave of reverse peristalsis and the relaxation of the pyloric sphincter and stomach
  • Forced inspiration, contraction of abdominal muscles and contraction of respiratory muscles occurs
  • LES relaxes, pylorus and antrum contract
  • UES relaxes
  • Contents of the stomach are expelled
  • Secondary peristalsis returns esophageal material back to the stomach because it senses distention of the esophagus and high acid content
23
Q

What are the key neurotransmitters that are involved in the emetic response?

A

Histamine, Ach, Serotonin (listed as 5-HT3), D2 (dopamine) are all important in emetic response.

24
Q

How do you treat motion sickness?

A

Interrupting Ach is very good at preventing motion sickness – like promethazine

25
Q

How is the physiology of the stomach altered in GERD?

A

Problems with any of the following mediators can cause an impairment leading to GERD

  • Histamine
  • Acetylcholine
  • Serotonin
  • Dopamine
26
Q

Describe gastroparesis

A
  • Gastroparesis means delayed gastric emptying – frequently associated with problems of pyloric sphincter or region.
  • It’s commonly seen in uncontrolled diabetes mellitus (due to neuropathy) – patients with this most likely have more stomach acidity problems because if motility in the pylorus region stops it from going out the bottom end, it’s more likely to come back out the mouth as the patient eats more (food builds up).
  • Gastroparesis is also frequently seen in infantile pyloric stenosis
27
Q

What neurotransmitters are involved in gastroparesis?

A
  • NO or VIP

- Vagal stimuli (dopamine, serotonin, histamine)

28
Q

Case study #3

A

Go read case #3

29
Q

How may diabetes contribute to the development of gastroparesis?

A

Diabetic neuropathy means loss of coordination in emptying as well as coordination in relaxation, churning, emptying. It doesn’t mean the stomach isn’t working – greater variability of what’s happening due to lack of coordination.

30
Q

Is his poor glycemic control a cause or consequence of gastroparesis?

A

Which came first, the chicken or the egg? Gastroparesis can cause diarrhea – less efficient absorption can impact retention of nutrients, ultimately impacting glycemic control. More likely though, the diabetic neuropathy caused gastroparesis – further supporting poor glycemic control. Seems kind of like a vicious cycle

31
Q

How can delayed gastric emptying cause diarrhea?

A

Think about this in the context of diabetes first. Maybe the lack of coordination means fast movement past through the duodenum (and subsequently bad absorption) but blockage at the level of pylorus. It could also mean many other things such as, releasing of the pylorus even when no food is anticipated or present – resulting in increased acid released into the duodenum and subsequent mucosal damage.

Physiology Exam 5 (10 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions