15 - Gastric Physiology, Acid Secretion, and Digestion Flashcards Preview

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1

Pancreas

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

2

Exocrine cells of the pancreas

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

3

Acinar cells

Secrete enzymes

4

Duct Cells

Secrete water, bicarb, sodium

5

Centroacinar cells

Cells that project back into the acini

6

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

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.

7

Secretin

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.

8

Cholecystokinin (CKK)

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.

9

What is the ideal pH fro pancreatic enzymes to work?

Neutral!

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

10

Secretin response to acid

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

11

Secretin's effect on the duct

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+

12

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

Gets more alkaline

13

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

Gets more acidic

14

What amplifies the absorptive surface of the gut?!

Length
Plicae
Villi
Microvilli
Glycocalyx

15

How big is the surface area of the intestines?

A tennis court!!!
300 square meters

16

Small intestinal mucosa crypt-villus organization

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.

17

Core of microvilli

Microfilaments

18

External plasma membrane surface of microvilli

Studded
Studs are clathrin, enzymes and transporters.

19

Terminal Web

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

20

Beneath the terminal web

Intermediate Filaments (providing structure)

21

Celiac Pathogenesis

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!

22

5 patterns of digestion-absorption

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)

23

Where are carbohydrates, proteins & lipids maximally absorbed?

Duodenum

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

24

Where are calcium, iron and folate actively absorbed?

Duodenum

Calcium also continues to be absorbed throughout small intestine.

25

Where are bile acids maximally absorbed?

Ileum

Less-so in the jejunum and the ascending colon

26

Where is B12 (cobalamin) absorbed?

ONLY IN THE ILEUM

27

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

B12 injections. Can't absorb it anymore.

28

Carbohydrate digestion

Luminal & Surface enzymes & transporters

Luminal digestion, terminating on the microvilli with immediate capture.

29

Carbohydrate Digestion - Luminal Enzymes

Amylase

30

Carbohydrate Digestion - Brush Border Enzymes

Glucoamylase
Lactase
Sucrase-Isomaltase

31

Carbohydrate breakdown products - Apical Transporters

SGLT1 (RIGHT NEXT TO Glucoamylase & Lactase)
GLUT5 (RIGHT NEXT TO Sucrase-Isomaltase

32

Carbohydrate breakdown products - Basolateral Transporters

GLUT2

33

SGLT1

Located on apical membrane. Sodium, sugar co-transporter

Na+ : Sugar
2 : 1

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

34

GLUT5

Apical transporter

Mainly in jejunum
Absorbs fructose

35

GLUT2

Basolateral membrane throughout small intestine

36

Intestinal epithelial cells - Na/K pump

Sodium into blood
Potassium into cell.

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

37

5 Pancreatic Peptidases

Trypsinogen
Chymotrypsinogen
Proelastase
Procarboxypeptidase A
Procarboxypeptidase B

38

Trypsinogen

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

39

Trypsin

Cleaves the inactive forms of all 5 pancreatic peptidases.

40

Chymotrypsinogen

Cleaved to Chymotrypsin by Trypsin

41

Proelastase

Cleaved to elastase by Trypsin

42

Procarboxypeptidase A

Cleaved to Carboxypeptidase A by Trypsin

43

Procarboxypeptidase B

Cleaved to Carboxypeptidase B by Trypsin.

44

Endopeptidases

Trypsin
Chymotrypsin
Elastase

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

45

Exopeptidases

Carboxypeptidase A
Carboxypeptidase B

Nibble peptides from the ends (single amino acids)

46

Protein Digestion

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

Amino acid absorption

Sodium-coupled transport at apical membrane

48

Protein Digestion - Luminal

Yields oligopeptides (and AAs that are absorbed)

49

PepT1

H+/Oligopeptide cotransporter

Those peptides are digested in the cytosol

50

Fat absorption

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

Acid microclimate disequilibrium zone

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

Chylomicron Absorption

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

53

Vitamin B12

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

Histo - Active Gastritis

Neutrophil Infiltration

55

Histo - Chronic Gastritis

Plasma Cells
Lymphocytes
Rare Eosinophils

56

Histo - Hemorrhagic Gastritis

Fresh Blood

57

Histo - Erosive Gastritis

Destruction of parts or entire mucosa

58

Histo - Granulomatous Gastritis

Granulomas

59

Histo - Eosinophilic Gastritis

Eosinophils

60

Histo - Lymphocytic Gastritis

Intraepithelial Lymphocytes

Oft associated with celiac disease

If not, lymphoma of the stomach

61

Histo - H. Pylori

"Chronic Active Gastritis"

Neutrophils
Plasma Cells
Lymphocytes
Rare Eosinophils

62

Autoimmune Gastritis

Autoantibodies to Parietal Cells
Rarely AutoAb to Intrinsic Factor

Body predominant inflammation (Lymphs, Plasma Cellz)

Antrum spared

Atrophy (loss of oxyntic glands)

63

Autoimmune Gastritis - Atrophy

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

Hypergastrinemia causes ECL hyperplasia