HRR: secretions and motility III Flashcards

1
Q

What are secretions of the LES and cardia?

A

Mucus and bicarb

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2
Q

What is unique about the cardia of the stomach?

A

It has the oblique layer of muscle in the ME. It helps the valve function of the LES

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3
Q

What are secretions of the fundus and body?

A

Protons, IF, mucus, bicarb, lipase, pepsinogens

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4
Q

What motility functions occur in the fundus and body?

A

Reservoir, tonic force during emptying

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5
Q

What are secretions of the antrum and pylorus?

A

Mucus and bicarb

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6
Q

What motility functions occur in the antrum and pylorus?

A

Mixing, grindings, regulation of emptying

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7
Q

What do surface epithelial cells do?

A

Secrete bicarb and mucous to protect the epithelium

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8
Q

What do mucus neck cells do?

A

Secrete mucus; higher in cardia and antral regions

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9
Q

What do parietal cells do?

A

Secrete HCL and IF. Higher amount in body and fundus

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10
Q

What do chief cells do?

A

Secrete pepsinogens

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11
Q

What do enterochromaffin cells do?

A

Secrete histamine

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12
Q

What do D cells do?

A

Secrete somatostatin

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13
Q

When are stomach acids produced?

A

Prior to the gastric phase; their production is initiated in the cephalic and oral phases from vagal stimulation

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14
Q

What are the stimuli for increased gastric acid secretion during the gastric phase?

A

Distension of the stomach and partially digested proteins or amino acids sensed by G cells

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15
Q

Describe what happens when food enters the stomach and causes distension.

A

The vagovagal reflex is activated, resulting in ach and GRP release that will lead to activation of parietal cells. Local ENS reflex pathways are also activated, leading to Ach release and further activation of parietal cells

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16
Q

Describe how partially digested proteins increase gastric acid secretion.

A

G cells sense the proteins and secrete gastrin that will act on parietal cells to increase HCL secretion. Enterochromaffin cells will secrete histamine and activate parietal cells

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17
Q

Which cells does vagal efferent outflow impact?

A

Parietal cells, ECL cells, G cells, and chief cells

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18
Q

How does the vagus nerve impact the stomach?

A

Through the enteric nervous system

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19
Q

What stimulates parietal cells to make acid?

A

Gastrin, ach, histamine

20
Q

What receptor in the parietal cell responds to gastrin?

21
Q

What receptor in the parietal cell responds to histamine?

22
Q

What molecules are inhibitory for parietal cells?

A

Somatostatin and prostaglandin

23
Q

Describe what happens to parietal cells upon stimulation to become activated.

A

They undergo cytoskeletal rearrangement, resulting in fusing of tubulovesicular and canalicular membranes. This increases their surface area. They also add a bunch of HK pumps, K channels, and Cl channels to the canalicular membrane

24
Q

How do parietal cells produce acid?

A

Water and CO2 enter the cell, where carbonic anhydrase forms carbonic acid. Carbonic acid dissociates into H and bicarb. The proton will be secreted into the lumen by the HK pump, and the bicarb gets exchanged into the blood

25
Q

What is the major pump for protons to move into the gastric lumen?

26
Q

What do D cells do?

A

Sense when the pH falls below 3. When this happens, they secrete somatostatin to inhibit gastrin secretion to decrease parietal cell function and HCL secretion

27
Q

What are some effects of somatostatin?

A

Splanchnic vasoconstriction, decreases pepsinogen secretion, reduces pancreatic enzyme and bile secretion, and overall reduces GI motility and gastric emptying

28
Q

What happens to gastric pH when we eat a meal?

A

It actually will initially drop! The food we eat is more neutral than stomach pH.

29
Q

What is a gastrinoma?

A

A neuroendocrine tumor that produces gastrin autonomously; it does not respond to negative feedback. This overwhelms the stomach and may lead to ulcers, heartburn, and diarrhea

30
Q

What is autoimmune atrophic gastritis?

A

Antibody and T cell mediated destruction of parietal cells that causes a lack of IF secretion leading to pernicious anemia as well as low HCl secretion that causes iron deficiency and high gastrin

31
Q

What can cause chronic atrophic gastritis?

32
Q

What is the main stimulator of chief cells?

33
Q

What is pepsinogen?

A

Inactive proenzyme of pepsin secreted by chief cells

34
Q

What is required for pepsinogen activation?

35
Q

When does pepsin become inactivated?

A

In the neutral environment of the duodenum

36
Q

Describe how NSAIDs impact the GI system.

A

They inhibit prostaglandin production. Normally, prostaglandins reduce gastric acid secretion and stimulate gastric mucus and bicarb secretion. Inhibiting prostaglandins leads to more stomach acid and potential damage to gastric epithelium

37
Q

How does the stomach achieve emptying?

A

Contraction of proximal and distal stomach and relaxation of pyloric sphincter

38
Q

What is adaptive relaxation?

A

Relaxation of the stomach in response to food entering

39
Q

Describe the process of adaptive relaxation.

A

Mechanoreceptors sense distension, leading vagal afferent nerves to signal the vagal ganglion, then vagal efferent nerves stimulating ENS to relax smooth muscle. The ENS itself will also stimulate interneurons followed by motor neurons to stimulate relaxation of smooth muscle

40
Q

Which portion of the stomach has thicker muscle: proximal or distal? Why?

A

Distal to aid in churning and mixing to create chyme

41
Q

What impacts the rate of gastric emptying?

A

Food composition, volume, medications, nerve/muscle conditions, and hormones

42
Q

Which macronutrient empties the fastest?

43
Q

Describe the process of gastric emptying.

A

As gastric contents become chyme, antral contraction and transient relaxation of the pyloric sphincter results in some entering the duodenum. The proximal stomach will increase tone and distal stomach contractions become more forceful to propel chyme into the transient openings of pyloric sphincter and into the duodenum. When pylorus is open, distal portion relaxes and chyme just flows

44
Q

What is the enterogastric reflex?

A

The process by which signals travel to the CNS resulting from duodenum sensing distention/fats, followed by signals back to the GI tract to stop gastric emptying, decrease gastric motility, and decrease gastric acid production

45
Q

What is gastroparesis?

A

Delayed emptying of the stomach due to damage to the stomach’s neural network and interstitial cells of cajal

46
Q

What is the most common cause of gastroparesis?