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GI / Hepatology > 15 - Gastric Physiology, Acid Secretion, and Digestion > Flashcards

15 - Gastric Physiology, Acid Secretion, and Digestion Flashcards

1
Q

Pancreas

A

Mixed endocrine-exocrine organ
Primarily exocrine
Acini = 84% Ducts, 5% of pancreatic mass
Islets (endocrine pancreas) = 1% of pancreatic mass
Both ducts and acini of the exocrine pancreas are secretory

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2
Q

Exocrine cells of the pancreas

A

Polarized
Secrete from apical surfaces
Respond to signals delivered to basolateral surfaces

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3
Q

Acinar cells

A

Secrete enzymes

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4
Q

Duct Cells

A

Secrete water, bicarb, sodium

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5
Q

Centroacinar cells

A

Cells that project back into the acini

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6
Q

Mechanism for creating bicarb that is eventually shuttled into the lumen of the duct

A

CO2 + H2O = HCO3- and H+

H+ moves into bloodstream in exchange for sodium
Sodium moves into the bloodstream in exchange for potassium via the Sodium/Potassium pump (sodium is kind of just a middle man)
Bicarb moves into the lumen in exchange for chloride.

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7
Q

Secretin

A

H+ stimulates secretin’s production.
Produced by S Cells
Stimulates cAMP (works with nerves, works without nerves)
Duct cells put out a lot of water and bicarb.

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8
Q

Cholecystokinin (CKK)

A

Produced by I cells
Stimulates duct cells to release intracellular calcium (via IP3 cascade, working together with nerves)
Calcium is the signal for pancreatic enzyme release.

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9
Q

What is the ideal pH fro pancreatic enzymes to work?

A

Neutral!

This means the pancreas has to secrete bicarb along with its enzymes so that the acidic pH of the gut can be combatted!

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10
Q

Secretin response to acid

A

Acid induces secretin-releasing peptides (S-RPs) to be released.
Vagal stimulation also induces this.
S-RPs stimulate S cells
S cells release secretin

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11
Q

Secretin’s effect on the duct

A

Secretin stimulates receptors on the duct cells.
Duct cells increase cAMP production.

Carbonic anhydrase catalyzes the production of H+ and HCO3- from CO2 and H2O
Luminal Cl- channel (CTFR) opens, and is coupled to a Cl-/HCO3- antiport channel.
Basolateral Na+/H+ antiport, Na+/K+ ATPase & H+ ATPase (exporting H+

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12
Q

Overal trend. When the gut gets more acidic (via parietal cells), the blood

A

Gets more alkaline

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13
Q

When the gut gets more basic (via pancreatic secretion), the blood

A

Gets more acidic

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14
Q

What amplifies the absorptive surface of the gut?!

A 
Length
Plicae
Villi
Microvilli
Glycocalyx
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15
Q

How big is the surface area of the intestines?

A

A tennis court!!!

300 square meters

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16
Q

Small intestinal mucosa crypt-villus organization

A

Crypt-villus axis is continuous (Cores of villi contain lamina propria)
Stem cells are found near the base of the crypts (generate crypt epithelial cells that line the villi)
Enterocytes mature at the crypt-villus junction
Old cells are extruded from villus tips.
It’s like an escalator.

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17
Q

Core of microvilli

A

Microfilaments

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18
Q

External plasma membrane surface of microvilli

A

Studded

Studs are clathrin, enzymes and transporters.

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19
Q

Terminal Web

A

Microfilaments in microvilli enter the cells and are linked by myosin. This is called the terminal web.

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20
Q

Beneath the terminal web

A

Intermediate Filaments (providing structure)

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21
Q

Celiac Pathogenesis

A

Gluten triggers a hypersensitivity reaction against the gut.
Crypt cells turn over crazy quicksies.
The intestines are now lined with crypt cells without the microvilli and junk!!!!!! Can’t absorb!!!!!!!!

Steatorrhea
Fat-soluble vitamin deficiencies!

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22
Q

5 patterns of digestion-absorption

A

No digestion (glucose transport)

Luminal hydrolysis of polymer to monomers (protein to AA, AA transport)

Brush border hydrolysis of oligomer to monomer (Sucrose to fructose & glucose, glucose & fructose transport)

Intracellular hydrolysis (peptide uptake, breakdown to AA, AA export)

Luminal hydrolysis followed by intracellular resynthesis (triglyceride to glycerol & fatty acids, uptake of those components, triglyceride resynthesis, triglyceride export)

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23
Q

Where are carbohydrates, proteins & lipids maximally absorbed?

A

Duodenum

Less absorbed further downstream, no more absorption once you hit the ileum.

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24
Q

Where are calcium, iron and folate actively absorbed?

A

Duodenum

Calcium also continues to be absorbed throughout small intestine.

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25
Q

Where are bile acids maximally absorbed?

A

Ileum

Less-so in the jejunum and the ascending colon

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26
Q

Where is B12 (cobalamin) absorbed?

A

ONLY IN THE ILEUM

27
Q

What MUST you do (nutritionally) if you’ve had to remove your ileum?

A

B12 injections. Can’t absorb it anymore.

28
Q

Carbohydrate digestion

A

Luminal & Surface enzymes & transporters

Luminal digestion, terminating on the microvilli with immediate capture.

29
Q

Carbohydrate Digestion - Luminal Enzymes

A

Amylase

30
Q

Carbohydrate Digestion - Brush Border Enzymes

A

Glucoamylase
Lactase
Sucrase-Isomaltase

31
Q

Carbohydrate breakdown products - Apical Transporters

A

SGLT1 (RIGHT NEXT TO Glucoamylase & Lactase)

GLUT5 (RIGHT NEXT TO Sucrase-Isomaltase

32
Q

Carbohydrate breakdown products - Basolateral Transporters

A

GLUT2

33
Q

SGLT1

A

Located on apical membrane. Sodium, sugar co-transporter

Na+ : Sugar
2 : 1

Doesn’t absorb L-glucose or fructose. D-form only!!

34
Q

GLUT5

A

Apical transporter

Mainly in jejunum
Absorbs fructose

35
Q

GLUT2

A

Basolateral membrane throughout small intestine

36
Q

Intestinal epithelial cells - Na/K pump

A

Sodium into blood
Potassium into cell.

Continues the momentum of the sodium that was co-imported with sugars by SGLT1

37
Q

5 Pancreatic Peptidases

A 
Trypsinogen
Chymotrypsinogen
Proelastase
Procarboxypeptidase A
Procarboxypeptidase B
38
Q

Trypsinogen

A

Cleaved by Enterokinase (enteropeptidase) on the brush border of the jejunum. Becomes Trypsin there.

39
Q

Trypsin

A

Cleaves the inactive forms of all 5 pancreatic peptidases.

40
Q

Chymotrypsinogen

A

Cleaved to Chymotrypsin by Trypsin

41
Q

Proelastase

A

Cleaved to elastase by Trypsin

42
Q

Procarboxypeptidase A

A

Cleaved to Carboxypeptidase A by Trypsin

43
Q

Procarboxypeptidase B

A

Cleaved to Carboxypeptidase B by Trypsin.

44
Q

Endopeptidases

A

Trypsin
Chymotrypsin
Elastase

Karate chops peptides into smaller ones (2 - 6 amino acids each)

45
Q

Exopeptidases

A

Carboxypeptidase A
Carboxypeptidase B

Nibble peptides from the ends (single amino acids)

46
Q

Protein Digestion

A

In lumen and at brush borders

Same deal as complex carbohydrates via pepsinogen/pepsin in stomach, then trypsin, chymotrypsin, elastase, carboxypeptidase A, carboxypeptidase B in the lumen of jejunum, then brush border peptidases finish off the oligopeptides, like maltotriose and junk

47
Q

Amino acid absorption

A

Sodium-coupled transport at apical membrane

48
Q

Protein Digestion - Luminal

A

Yields oligopeptides (and AAs that are absorbed)

49
Q

PepT1

A

H+/Oligopeptide cotransporter

Those peptides are digested in the cytosol

50
Q

Fat absorption

A

Hydrolysis & resynthesis

In lumen, bile salts detergentrify the emulsion droplets and enzymes break down the triglycerides, forming a mixed micelle.

Triglycerides hydrolyzed to glycerol and fatty acids.

Those components are absorbed

Triglycerides reassembled in Endoplasmic Reticulum (Technically “outside” the cell).

They meet up with apoproteins from the RER.

These complexes are processed and packaged in the golgi, and exported as a chylomicron.

Released via Exocytosis!

51
Q

Acid microclimate disequilibrium zone

A

Acidic region of the lumen adjacent to the microvilli, maintained by Na+/H+ pump.

This allows for monoglycerides and fatty acids to move across the membrane easily.

52
Q

Chylomicron Absorption

A

Lymphatics have discontinuous walls that allow for absorption. This dumps into the thoracic duct, and back into circulation.

53
Q

Vitamin B12

A

Eat B12 bound to food.

Stomach acid dissociates B12 from food.

Haptocorrin (made by gastric and salivary glands) binds to B12 to protect it from stomach acid.

Haptocorrin-B12 and Intrinsic Factor travel to the duodenum.

Trypsin, chymotrypsin and elastase digest Haptocorrin, allowing B12 and IF to complex.

Terminal ileum contains IF-B12 receptors. Endocytose complex

Lysosomes fuse and digest IF, allowing B12 to enter the cytoplasm.

B12 enters secretory vesicles containing Transcobalamine II, which complexes with B12 and is secreted into the interstitial space.

54
Q

Histo - Active Gastritis

A

Neutrophil Infiltration

55
Q

Histo - Chronic Gastritis

A

Plasma Cells
Lymphocytes
Rare Eosinophils

56
Q

Histo - Hemorrhagic Gastritis

A

Fresh Blood

57
Q

Histo - Erosive Gastritis

A

Destruction of parts or entire mucosa

58
Q

Histo - Granulomatous Gastritis

A

Granulomas

59
Q

Histo - Eosinophilic Gastritis

A

Eosinophils

60
Q

Histo - Lymphocytic Gastritis

A

Intraepithelial Lymphocytes

Oft associated with celiac disease

If not, lymphoma of the stomach

61
Q

Histo - H. Pylori

A

“Chronic Active Gastritis”

Neutrophils
Plasma Cells
Lymphocytes
Rare Eosinophils

62
Q

Autoimmune Gastritis

A

Autoantibodies to Parietal Cells
Rarely AutoAb to Intrinsic Factor

Body predominant inflammation (Lymphs, Plasma Cellz)

Antrum spared

Atrophy (loss of oxyntic glands)

63
Q

Autoimmune Gastritis - Atrophy

A

Loss of parietal cells in oxyntic glands causes Hypergastrinemia!!!

Hypergastrinemia causes ECL hyperplasia

GI / Hepatology (28 decks)

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