GI 4 Flashcards

1
Q

Primary process of acid secretion from parietal

A
  1. Free H+ actively transported across apical membrane
  2. Water dissociates to H+ and OH- freeing more H+ to be actively transported out
  3. OH- combines with CO2 via CA to generate HCO3
  4. HCO3 exchanged with Cl at basolateral
  5. Cl diffuses across apical through open channels
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2
Q

What can the primary mechanism of acid secretion create

A

A lot of HCO3 in interstitial which can cause significant shift in pH of blood leading stomach
- short lived because pancreas

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3
Q

What is secondary mechanism of acid secretion

A

CO2 joins H20 to become H2CO3 which dissociates to H+ which is regularly transported across apical and HCO3 transported across basolateral

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4
Q

What happens with endocytosis of apical membrane of parietal cell

A

Channels internalized and cells not very active, cannot secrete a lot of H+

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5
Q

What is the stimuli for acid secretion

A

Insertion of apical H+/K+ ATPase, Cl- and K+ transported stored in vesicles
Stimuli causes exocytosis and insertion of transporters which turns on acid secretion

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6
Q

What is the negative regulator of acid secretion

A

Somatostatin

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7
Q

What is excessive acid treated with

A

H2 receptor antagonists or proton pump inhibitors (H-K ATPase)

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8
Q

What can inhibit acid secretion

A

Somatostatin
Intestinal hormones
Meds

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9
Q

What is the short reflex of gastric acid secretion

A
  • once food enters stomach (further reinforced)
  • luminal distension, AAs and peptides increase gastrin secretion which stimulate parietal cells
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10
Q

What is long reflex of gastric acid secretion

A

Cephalic phase (sight, though,etc)
Brain cause increase ENS activity
Stimulates G cells, ECL cells, parietal cells
Increases HCl

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11
Q

What can increased HCl stimulate

A

D cells to increase somatostatin secretion to affect acid secretion

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12
Q

Gastric digestive enzyme secretion process

A

Chief cells release pepsinogen and gastric lipase
Pepsinogen cleaved to pepsin by HCl
Pepsin breaks down protein to peptides

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13
Q

What is gastric digestive enzymes stimulated by (secretion by chief cells)

A

Acid secretion via short reflex

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14
Q

What does ECL release of histamine activate

A

H2 receptors on parietal cells to stimulate HCl secretion

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15
Q

What does parietal cells release of intrinsic factor form

A

Complex with vit B12 so it can be absorbed

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16
Q

What does D cells activation of somatostatin cause

A

Negative feedback for acid secretion (G cells, parietal cells, and ECL)
Inhibits pepsinogen release (inhibit chief cells)

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17
Q

Food or cephalic reflexes initiate gastric secretion of what

A

Gastrin, histamine, and acid

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18
Q

Gastrin stimulates what

A

Acid secretion by direct action on parietal cells

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19
Q

What is indirect sitmulus of parietal cells

A

Histamine

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20
Q

Acid stimulate what

A

Short reflex secretion of pepsinogen

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21
Q

Mucus and HCO3 secreted from

A

Mucous cells (to prevent breakdown of epithelial cells)

22
Q

What is mucus secretion stimulated by

A

Parasympathetic input and irritation

23
Q

What is HCO3 secretion stimulated by

A

Parasympathetic input and H+

24
Q

What are the 2 mucous cell types

A

Mucous surface cell
Mucous neck cell

25
What is the physical barrier
Mucus layer
26
What is the chemical barrier that neutralizes acid
Bicarbonate
27
What is a peptic ulcer
Sore or break in lining of stomach or duodenum (acid + digestive enzymes break down)
28
What is peptic ulcers caused by
Excessive acid production (gastrin secreting tumors) Nonsteroidal anti-inflammatory drugs (chronic use, aspirin, ibuprofen) H. Pylori
29
What was believed to cause ulcer
Stress, spicy foods, over production of acid
30
What was finally hypothesized to cause ulcers
Bacteria
31
How does H.pylori cross mucus layer
Urease inside breaks down urea into NH3 and CO2 Creates buffer zone around themselves Buffer attracted to HCO3 and mucus layer Mucus layer breaks down and exposes epithelia
32
How much food, fluid, secretions enter small intestine
5.5 L and additional 3.5 L added from hepatic, pancreatic, and intestinal
33
Why is motility in small intestine regulated
To ensure proper digestion and absorption
34
What type of contraction mix chyme in small intestine
Combination of segmental and peristaltic
35
What does contractions in sm int cause
Mix chyme with enzymes Expose nutrients to mucosal epithelium for absorption
36
Where is most absorption in sm int
7.5L in duodenum and jejenum (most in jejenu)
37
What promotes and inhibits motility in sm int
Parasympathetic innervation, gastrin, and cholecystokinin promotes Sympathetic innervation inhibits
38
What increase surface area in sm int
Plicae (large folds), villi, microvilli
39
What do villi do
Increase surface area available for absorption and secrete mucus (goblet cells)
40
What do crypts do
Contain hormone and fluid secretory cells and stem cells
41
Where are most nutrients in sm int absorbed into
Capillaries in villi
42
What do lateals of lymph vessels transport
Most fats to lymph
43
What are brush border enzymes
Enzymes stay attached to microvilli
44
Where does venous blood go from GI tract
Hepatic portal system Liver acts as biological filter
45
What does the liver acting as biological filter do
Contains variety of enzymes that metabolize drugs and xenobiotics and clear them from the blood stream before it proceeds to systemic circulation
46
Why do drugs given orally have higher dose then IV
Absorbed in GI then metabolized in liver then travels through systemic
47
How much secretions enter lumen of sm int
3.5 L
48
What 5 types of secretions enter sm it
Digestive enzymes (brush border and pancreas) Bile Bicarbonate (pancreas) Mucus (goblet cells) Isotonic saline (crypt cells)
49
What do mucus and isotonic saline do
Lubricate contents of gut
50
How is isotonic saline produced
1. Na, K+, and CL- enter by cotransport 2. Cl enters lumen through CFTR 3. Na+ is reabsorbed 4. Negative CL in lumen attracts Na by paracellular pathway 5. Water follows