GI phys Lecture 2 Flashcards

1
Q

Difference between segmentation and Peristalsis

A

Peristalsis: involves smooth muscle / longitudinal muscle interaction, moving contents forward. Propulsion.

Segmentation: purpose is to mix contents. Promotes digestion

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2
Q

Secretion:

Acinar Cells / Duct cells

A

Acinar cells connected to duct cells, both are polarized. (transporters are different from apical and basolateral).

Acinar cells: synthesize / secrete pdts.

Duct cells: transport fluid / electrolytes

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3
Q

Increase of flow rate, what happens?

A

Na increases, plateaus
HCO3- (bicarbonate) increases, plateaus
Cl- increases, linear
K+ decreases, plateus

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4
Q

Sjogren Syndrome

A

Difficulty in tasting/chewing/swallowing/speaking

Dry mucosa, parotid glands enlarged. Autoimmune disorder

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5
Q

LES and cardia, what is there

A

Mucus and Bicarbonate.

Bicarbonate there to maintain pH bc u don’t want acid in esophagus

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6
Q

Fundus and upper body secretions

A

H+, intrinsic factor, mucus, bicarbonate, pepsinogen and lipase

has parietal cells that secrete HCl

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7
Q

Antrum and lower body contain…

A

Mucus and bicarbonate

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8
Q

Tubulovesicles

A

Contain H+, K+ ATPase, morphological change occurs, making canaliculus have more surface area from resting to secreting. In parietal cells.

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9
Q

Apical (lumen) transporters of Parietal cells

A

H / K exchanger
K and Cl can leave through channels

Does not secrete HCl directly, secretes H+ ions and Cl-

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10
Q

Basolateral transporters of Parietal cells

A

HCO3- / Cl-
Na / K
CO2 can come from blood / plasma

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11
Q

Which receptors are stimulatory and inhibitory for parietal cells? Which are the secondary messengers associated with these?

A

Basolateral receptors of ACh, gastrin, histamine stimulate parietal cells, secreting HCl.

M3 = ACh
H2 = Histamine
CCK-B = Gastrin

ECL cell make histamine

Somatostatin (SST) from D cells is ALWAYS inhibitory.

Ca++ for ACh and Gastrin, cAMP for Histamine are the secondary messengers

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12
Q

Mechanism of G cells in Antrum

A

GRP (gastrin releasing peptide) stimulates G cells which makes Gastrin which stimulates parietal secretion of HCl.

D cells stimulate SST which inhibit G cell production of Gastrin.

Note that Gastrin is not a NT (it is a GI hormone) and must be transported via blood.

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13
Q

PPI (proton pump inhibitor) mechanism

A

Inhibits final step, H+ K+ ATPase in parietal cells.

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14
Q

Effects of H. Pylori and how it affects gastric mucosa:

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A

Increase NH3 production
Decrease number antral D cells
Increase prod. of gastrin
Increase acid secretion
Inflammatory responses release cytokines

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15
Q

Effects of NSAIDS and how it damages gastric mucosa
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A

Less mucous and bicarbonate production, increase gastrin secretion, decrease gastric blood flow, neutrophils release free radicals and proteases.

NSAIDS inhibit prostaglandins, u need prostaglandins for healthy gastric mucosa.

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16
Q

3 agents that stimulate pancreatic secretion

A

CCK, secretin, ACh.

Vagal nerve fibers responsible for ACh.

17
Q

Difference between CCK and Secretin

A

CCK primary affect on acinar cells, Secretin primarily duct cells.

Secretin causes production of bicarbonate as a buffer, cholecystokinin promotes synthesis of enzymes.

Both are GI hormones and thus must be transported by blood.

18
Q

Acute / Chronic Pancreatitis facts

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A

Gallstones / alcohol consumption cause this. Gallstones can cause fluid from pancreas to back up. Fluid containing enzymes can start digesting the pancreas.

19
Q

How to have constriction behind of a bolus:

How to have relaxation on other side of bolus:

A

Propulsive segment: Circular muscle contracts, longitudinal muscle relaxes. Inhibitory motor neurons are off

Receiving segment: Relaxation of circular muscle, contraction of longitudinal. Inhibitory motor neurons are on.

20
Q

Gastro colic reflux

A

Connection between motility pattern in the colon and what goes on in the stomach

Mass movement / Segmentation can occur after you eat a meal.