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Gastic secretion Flashcards

1
Q

How does the stomach participate in protein digestion>

A

acid hydrolysis and pepsin cleavage

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2
Q

How does the contents from the stomach enter the SI?

A

at a controlled rate to optizmize further digestion and absoprtion

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3
Q

Bezoar

A

ball of foreign material trapped in stomach (hairball)

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4
Q

Emesis

A

Vomiting, forcible ejection of stomach contents through the mouth

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5
Q

Dyspepsia

A

indigestion, pain in upper abdomen after eating

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6
Q

Gastroparesis

A

delayed emptying

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7
Q

Migrating Motor Complex

A

clears undigested material from the GI tract

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8
Q

Regurgitation

A

flow of material that has not reached the stomach back up the esophagus

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9
Q

Rugae

A

Stomach folds which expand as stomach fills

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10
Q

Scintigraphy

A

using a dual-radiolabeled solid and nutrient liquid meal, to measure gastric emptying

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11
Q

Trituration

A

grinding of food into small molecules

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12
Q

Paritel cell secretes

A

HCL, IF (for B12 absoprtion in the ileum)

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13
Q

Chief cells secrete

A

pepsinogen for protien digestion

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14
Q

surface mucous cells secrete

A

mucus, HCO3 fir gastroprotection

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15
Q

G cells in the antrum secrets

A

gastrin which activate parietall cells in the fundus to secrete acid

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16
Q

What kind of receptor does gastrin bind to

A

CCK2

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17
Q

what triggers gastrin release from the g cells in teh antrum?

A

seeing food or stomach distention causes vagal stimulation, causing gastrin releasing peptide, aromatic AA in the lumen

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18
Q

What activates parietal cells?

A

gastrin, histamine, and AcH

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19
Q

What activates ECL cells?

A

AcH, gastrin

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20
Q

ECL cells release what?

A

histamine which then binds to parietal cells

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21
Q

What happens upon parietal stimulation?

A

tubulovesicular membranes fuse with canalicular membranes increasing the density of H+, K+ ATPase molecules at the apical membrane.

22
Q

Describe the ion transport of the parietal cells

A

Protons are made in the cytosol and pumped out via - H+, K+ ATPase into the lumen, bicarb in exported in from the basolateral (blood) side by vesiscular fusion/CH/HCO3 exchanger and enters blood stream

23
Q

How does Cl move during parietal cell stimulation>

A

passive from basolateral side to lumen, water follows

24
Q

What is the electrical potential exists across the gastric mucosa at rest? during activation?

25
What inhibits gastrin release?
somatostatin which is secreted from D cells in the atrum when the pH is <3
26
What happens during the gastric phase?
You get an icnrease in pH due to food which decreases somatosatin secretion
27
what does somatisatin inhibit?
Inhibits formation of cAMP(prostiglandins also do this) via a Gi-dependent signaling pathway in parietal cells, indirectly inhibits ECL secretion of histamine, G cells release of gastrin
28
What does the feedback from the duodenum do to parietal cells
nervous reflux blocks activation of parietal cells, enterogastrones like secretin block secretion of histamine by ECL cells
29
What is the Interdigestive Phase
Low acid secretion, D cells secrete somatostatin to maintain low levels of Gastrin
30
Cephalic Phase
dorsal vagal complex integrates input from higher centers (seeing and tasting food) to activate Vagus nerves. GRP activates gastrin release and Ach activates ECL and parietal cells.
31
Gastric Phase
distension of the stomach activates vagal afferents and the enteric nervous system. Amino acids activate gastrin secretion and food raises pH decreasing somatostatin secretion.
32
Intestinal Phase
introduction of the gastric contents into the small intestine activates duodenal G cell secretion of gastrin. Activation of secretin and other enterogastrones and neural reflex decreases secretion.
33
Do PPI have an effect on intrsic factor?
NO! can still absorb b12
34
What can cause a lack of B12 absoportion
autoimmune destriction of parietal cells, BYPASS SURGERY! can get megablastic anemia and neurological defects
35
What secretes pepsinogen? in response to what
chief cells, AcH and gastrin,
36
what inhibits pepsingen secretion?
secretin
37
what kind of molecule is pepsinogen
inactive prozyme proteases, activated by acid
38
what kind of molecule is pepsin
endopeptidase, can further activate pepsinogen by autolysis
39
What do surface epithelial cells secrete?
mucus and bicarb in response to PGE2
40
What effect does NSAIDS have on muscus seretion?
It decreases it since it blocks PGE2, this contributes to gastric irritation
41
What can catecholamines do to gastric mucosa?
suppress bicarb secretion, this contributes to gastric ulcers- STRESS ULCERS!
42
How do you regenerate disrupted epitheloum?
by using trefoil factors and growth factors
43
What is Zollinger Ellison Syndrome?
its a gastrin secreting tumor in the pancrease or intestine, excess H secretion as well as hyperplasia and hypertrophy of parietal cells, treat with PPi?
44
Peptic ulcer disease is due to?
hyperacidity, deterioration of the gastro musocsal barrier, get increase bleeding,
45
Some causes of gastric and duedenal ulcers
Infection – Helicobactor pylori Poor secretion of mucus, bicarbonate by the surface epithelium Stress (may contribute but doesn’t cause) Irritation by alcohol, acid, digestive enzymes, bile
46
Tx ulcers with>
antibiotics (amoc/cipro) and proton pump inhibitor. Stop NSAID
47
what is the pathophysiology of peptic ulcers?
increased gastin levels because somatostain is not active in fasting state, causes increase acid, pepsin, hyperplasa of ECL cells,
48
Peptic ulcers in patients with hypochlohydria is related to?
gastritis and destruction of gastric epithelial cells, decrease of acid production?
49
Achlorhydria is due to
reduced acid secretion, caused by aging, autoimmune attack of H/K atpase, PPI, infection, atropic gastritis,
50
Side effects of achlorhydria?
increase bacteria growth, HIP fractures due to decrease CA, FE def anemia, decreased pep, increased diarrhea

GI week 2 (8 decks)

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