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GI- Week 2 > Prunuske: Gastric Physiology and Motility > Flashcards

Prunuske: Gastric Physiology and Motility Flashcards

1
Q

What happens in the stomach as food enters?

A

Gastric mechanoreceptors trigger the swallowing reflex and cause the fundal wall to undergo receptive relaxation so the stomach can store 2-4 L!

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2
Q

What can alter receptive relaxation and gastric secretion of the stomach?

A

Dorsal vagal complex (CNS input)

Sympathetic input in response to a meal

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3
Q

Which NT are released during receptive relaxation?

A

Para (DVC)- ACh> induces relaxation NOT contraction

VIP/NO>

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4
Q

Expansion of the stomach signals what?

A

Forward to empty the more distal segments through the gastrocolic and gastroileal reflex

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5
Q

What is the gastrocolic reflex?

A

induces the need to DEFECATE after ingesting a meal

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6
Q

What is the gastroileal reflex?

A

causes ileoceccal valve to relax and transfer contents from small to large bowel

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7
Q

How does low pH, pepsin endopeptidase, gastric lipase and mechanical movements aid the digestion process?

A

Low pH facilitates PROTEIN denaturation

Pepsin endopeptidase releases PEPTIDES

Gastric lipase (optimal at pH 3-6) produces free FA (G cells)

Mechanical movements are important for EMULSIFICATION

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8
Q

How are lipid soluble substances like alcohol and aspirin absorbed?

A

Diffusion

There is NO active transport

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9
Q

What facilitates gastric titration (mixing of the stomach) of liquids vs solids?

A

Liquids–Proximal stomach (reservoir) (tonic)

solids–antral pump (phasic) (mixing and grinding)–> some closing to make sure only small molecules can get through

**food must be smaller than 2 mm in diameter to pass through the pylorus

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10
Q

What type of gastric motility patterns are used to mix, titurate and sieve gastric contents?

A

Phasic contractions (3 cycles/min) that can generate waves

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11
Q

Describe how your stomach acts like a blender by explaining the cycle of contraction in the stomach.

A
  1. A circumferential contraction, A, sweeps toward the pylorus (which is closed) resulting in anterograde and retrograde propulsion of material.
  2. As contraction A subsides, a second contraction, B, mixes contents further.
    3. Contraction B is sufficient to cause transient and partial OPENING of the pylorus, allowing small particles to exit the stomach. Larger particles are propelled back into the stomach to be further dispersed by contraction C.
  3. Further cycles of contraction against a closed pylorus continue mixing and grinding until all of the meal is emptied from the stomach.
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12
Q

What causes peristalsis in the stomach?

A

Parasympathetic stimulation and distension activates AP. Pacemaker region in the body leads to regular changes in the membrane potential.

BER (3-5/min in the stomach) establishes the maximum frequency of the wave that is propagated over the stomach

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13
Q

How can you alter the amplitude of hte BER?

A

Both Neural (ACh –> Ca influx) and Hormonal (gastrin) input

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14
Q

What determines the magnitude of the peristaltic contraction?

A

Number of AP on teh crests of the slow waves

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15
Q

What happens to peristaltic contractions as they approach the closed pyloric sphincter?

A

strengthen and speed up

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16
Q

What causes rapid emptying of the stomach?

A

Rapid emptying is caused by tonic contractions of the reservoir (1a), deep
peristaltic waves along the gastric body (1b), deep constrictions of the antral
waves (2), a wide opening of the pylorus (3), a duodenal receptive relaxation (4)
and peristaltic duodenal contractions (5).

Pylorus more open, duodenum more relaxed

17
Q

What causes delayed emptying of the stomach?

A

Delayed emptying due to feedback inhibition is caused by a prolonged
relaxation of the reservoir (6a), shallow peristaltic waves along the gastric body
( 6b), shallow antral waves (7), a small pyloric opening (8), a lacking duodenal
relaxation (9) and segmenting duodenal contractions (10)

Relaxation or reservoir, pylorus closed more, duodenum more contracted

18
Q

What does the rate of emptying depend on?

A

The meal!

Glucose> protein> solid (fat)

19
Q

What inhibits gastric contractions and gastric emptying (slows things down!)?

A
  • acid in the duodenum via neural (enteric and vagal) and hormonal (secretin and somatostatin) mechanisms
    - fat in the duodenum via hormonal (CCK) mechanisms and via enteric neural mechanisms
    - increased osmolarity of the duodenal contents via enteric neural mechanisms and perhaps hormonal mechanisms
20
Q

How does feedback from the small intestine lead to delayed emptying?

A
  1. Fat> CCK> digestive enzymes, inhibits gastric motility> relaxation of fundus and decreases contractions
  2. Acid> secretin> secretion of bicarb from pancrease and decreases acid secretion and gastric motility
  3. Osmolarity (unsure of mechanism)
21
Q

What does the MMC do?

A

housekeeping function to remove indigestible material during fasting induced by MOTILIN

22
Q

What are the phases of the MMC?

A

Phase I: Quiescence
20-60 minutes

Phase II: Irregular,
Peristaltic Contractions
10-30 minutes
Increase in gastric, pancreatic juices

Phase III: MOTILIN (some drugs work like motilin)
Intense Contractions
5-10 minutes
Pylorus opens fully
Stimulated by some prokinetic drugs
23
Q

What is pyloric stenosis? How do you treat it?

A

congenital condition where pylorus fails to relax after a meal leading to malnutrition and dehydration. Can’t transfer chyme between stomach and SI.

Treated with surgical myotomy.

24
Q

What is gastroparesis? How do you treat it?

A

Reduced gastric emptying often due to DIABETIC neuropathy involving the vagus and enteric nerves in the stomach such that the stomach fails to generate enough force to empty the stomach.

Other causes include surgery, drugs, cancer treatments.

Results in nausea, vomiting, bloating, poor digestion, weight loss, malnutrition, impaired absorption of medications, and impaired glycemic control.

Treat with prokinetic drugs (stimulate clearing out of stomach contents)

25
Q

What is Dumping Syndrome?

A

Rapid gastric emptying often resulting from gastric by-pass surgery, vagotomy, and high sugar-containing meals.

Rapid entry of gastric contents into the duodenum represents an OSMOTIC challenge, water moves into the lumen resulting in hypovolemia and reduced blood pressure.

Results in nausea, weakness, dizziness, sweating, shakiness, diarrhea, heart palpitations

26
Q

What is peptic ulcer disease?

A

Scarring and ulcers near the pylorus can delay emptying or in duodenal ulcers can lead to rapid gastric emptying due to loss of duodenal negative feedback mechanisms.

27
Q

What causes emesis?

A

Causes: gastritis, poisoning, brain tumors, increased intracranial pressure, migraine, vestibular problems, bowel obstruction … etc

28
Q

What are emetic stimulants?

A

Stimulation of the pharynx, sensory input from higher centers, vestibular information, irritants or blockage in the GI tract

29
Q

What coordinates the mechanism for vomiting?

A

vomiting center in the medulla

30
Q

Why does increased salivation preceed vomiting?

A

Parasympathetic activation (bicarbonate) to protect the enamel of teeth from dental erosion

31
Q

How does vomiting occur?

A

Retro peristalsis, starting from the middle of hte small intestine, sweeps up the contents of the digestive tract into the stomach and through the RELAXED pyloric sphincter.

Retching (sequence but no vomiting UES is not open)

32
Q

What happens to the glottis, hyoid, diaphragm and abdominal muscles during vomiting?

A

Glottis closes to prevent aspiration of vomitus, hyoid moves upward and forward opening upper esophageal sphincter, contract diaphragm and abdominal muscles propelling stomach contents into the esophagus as the lower esophageal sphincter relaxes.

33
Q

What are the consequences of vomiting?

A

dehydration and electrolyte imbalance

34
Q

What is used to suppress vomiting?

A

Inhibitors of dopamine, histamine and serotonin

GI- Week 2 (11 decks)

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