GI secretions/digestions [4] Flashcards

1
Q

What secretes Gastric acid?
What is GA and what does it do?
Is it passive or does it require E?

A

Secreted by parietal cells ( contains HCl and IF)

Kills bacteria
Begins protein digestion (denature prot + activates pepsinogen → pepsin)

E consumin processs (H+/K+ ATPase pumps across luminal surface against significant gradient)
- knows its getting E back via digestion

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2
Q

4 phases of gastric secretion

A

basal phase + 3 assoc w/ eating

  1. interdigestive (basal) phase
  2. cephalic phase
  3. gastric phase
  4. intestinal phase
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3
Q

interdigestive (basal) phase of gastric secretion

A

between meals, following circadian rhythm

  • highest in the evening
  • lowest in the morning prior to waking
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4
Q

Cephalic phase of gastric secretion

A

neuronal control
- vagus

Cause:

  1. release of ACh
  2. trigger Histamine release from ECL cells
  3. release of GRP form vagal and ENS
  4. inhibition of somatostatin release form Delta cells
  • 30% of acid secretions
    (note: somatostatin a hormone secreted in the pancreas and pituitary gland that inhibits gastric secretion - so you inhibit an inhibitor)
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5
Q

gastric phase of gastric secretion

A

initially neural, followed by endocrine (gastrin) and neural reg.

  1. Food enters stomach
  2. distends gastric mucosa
  3. activates vasovagalreflex + local ENS reflexes
  4. partially digested proteins stimulate ANTRAL gastrin (G) cells
  5. release gastrin (50-60% of total acid secretion)
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6
Q

Intestinal phase of gastric secretion

A

mostly endocrine (largely inhibitory, telling us 2 stop prod acid)

  1. presence of aa and partially digested peptides in proximal small intestine
  2. stimulate acid secretion by stimulating DUODENAL gastrin (G) cells to secrete gastrin (5-10% of total acid secretion)
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7
Q

How do parietal cell secretagogues induce acid secretion

A

ACH → M3 receptor → ↑ intracellular Ca2+
Histamine → H2 receptor → ↑ intracellular Ca2+
gastrin → CCK3 receptor → ↑cAMP

These receptors in the basolateral membrane of parietal cells, potentiate gastric acid secretion (on lumenal side) when stimulated concurrently

  • one of the most E costly of any electrolyte transport process in body.
  • Together, Ca2+ and cAMP activates protein kinases to phosphorylate H/K+ ATPase
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8
Q

Direct/Indirect pathway of stimulating parietal cells to secrete gastric acid

A

direct pathway: ACh, His, Gastrin directly stim parietal cell

Indirect pathway: “ “ stimulate enterochromaffin like (ECL) cells to result in secretion of His → acts on parietal cells

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9
Q

Mech of gastric acid generation + secretion.

Role of: K+, Cl/HCO3, carbonic anhydrase, H+K+ ATPase

A
  1. H+ is actively transported across APICAL memb (←)
    in exchange for K+ by H/K ATPase (→)
    - when H+ moves out of cells (←) [HCO3-] in cells goes ↑
  2. HCO3- is transported across BASOLATERAL memb (→)
    in exchange for Cl- (←)
  3. Cl- that accumulates is transported across APICAL memb (←←) by facilitated diff
  4. H2O follows Cl-
    - pH of venous blood leaving stomach is high (HCO3- transport, known as ALKALINE TIDE)

(NOTE: all of this depends on Na/K ATPase, creating electronegative gradient (inside more neg than outside)

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10
Q

How does mucous serve as a protective barrier?

A

mucous secreted by goblet cells and mucous neck of the gland → form unstirred gel layer in which H2O is trapped + serves as neutralization zone for acid to be neutralized when diffused in

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11
Q

Peptic ulcer disease risk factors

A
  1. NSAIDs (block cox I → ↓ PG → ↓ mucous)
  2. Tumors (ZE synd)
  3. H. Pylori
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12
Q

First step of carbohydrate digestion takes place in the ______ with the enzyme ______.

Final step in carbohydrate digestion occurs at _____ for all dietary carbs

A

Mouth - amylase

enterocyte surface

(note that amylase digests digest starch polysacc α-1,4 bonds to sugars that eventually → glucose)

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13
Q

Digestion of proteins starts _______ from the enzyme, ______ and is completed in the ______ with the enzyme ______.

A

stomach - pepsin

small intestine - gastric, pancreatic, enterocyte brush border and cytoplasmic peptidases

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14
Q

Only monomeric _____ can be absorbed

A

SUGARS!!!

unlike proteins

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15
Q

Fat digestion starts in the mouth with the enzyme ____.

It ends in the ______.

A

fat - lingual lipase

duodenum/jejunum

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16
Q
Brush border enzymes involved at enterocytes:
Maltase acts on \_\_\_\_\_ or \_\_\_\_\_ → \_\_\_\_\_\_\_
Isomaltase (SI) acts on \_\_\_\_\_\_ → \_\_\_\_\_\_\_
Lactase acts on \_\_\_\_ → \_\_\_\_\_+ \_\_\_\_\_
Sucrase acts on \_\_\_\_ → \_\_\_\_\_+ \_\_\_\_\_
A

Maltase: maltose or maltotriose → Glucose
Isomaltase (SI): alpha limit dextrin → Glucose
Lactase Lactose → Glucose + galactose
Sucrase: Sucrose → Glucose + fructose

17
Q

Predict small int. and colonic consequences of a deficiency in brush border enzyme, lactase following dairy product consumption.

A
  1. unabsorbed lactose will draw water into intestinal lumen → osmotic diarrhea
  2. Gut bacterial flora metabolizes unabsorbed lactose → gas (H+, methane, CO2)
18
Q

Apical, brush border, sugar monomer transporters of enterocytes
- regulates uptake of?

A
  1. SGLT1: regulates uptake of glucose and galactose
  2. GLUT5: regulates uptake of fructose
    (moves from lumen INTO cell)
  • both are Na+ dependent (goes in with Na+ - cotransport)
19
Q

Basolateral, brush border, sugar monomer transporters of enterocytes
- regulates uptake of?

A

GLUT2: regulates glucose, galactose, and fructose
(moves OUT of cell into blood on basolateral side)

  • not Na+ dependent
20
Q

Which of the brush border transporters can operate in the setting of secretory diarrhea like in cholera?

A

SGLT1
Na+ and Glucose → into cell
Important in oral rehydration