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Describe motor patterns of the stomach after a meal.

Vago-vagal reflexes
- dilates to accommodate large volumes
- exhibits contractions for mixing food w/ gastric juice
- moves chyme into duodenum

Retropulsion

like a wave against rocks

- pushes chyme against closed pyloric sphincter

What are the exocrine secretions in stomach?

1. HCL
2. Pepsinogen
3. Mucus
4. Bicarbonate
5. Intrinsic Factor
6. Gastric Lipase
7. Water

What are the endocrine secretions in stomach?

1. Gastrin
- G cells
- stimulates acid production

2. Somatostatin
- D cells ("defense" or inhibitory cell)
- inhibits acid productions

What are the functions of the stomach?

HCL

Parietal Cells

- denatures proteins
- kills micro-organisms
- cleaves pepsinogen

Pepsinogen

Chief cells

- cleaved to make PEPSIN

Mucus

Mucous neck cells

- lubricates food
- forms gastric mucosal barrier protecting against acid and pepsin

Bicarbonate

Mucous neck cells

- forms gastric mucosal barrier
- counteracts acid

Intrinsic Factor

Parietal cells

- needed for Vit B12 absorption in ileum

Gastric Lipase

Chief cells

- fundus
- triglyceride hydrolysis
- acidic pH optimum

Water

- 1-2 liters per day
- dilute and dissolve ingested food

Restitution

rapid regeneration of epithelial gut cells due to gut stem cells

Location of cells in gastric lumen

Is gastric juice isotonic to plasma at ALL flow rates?

YES

What is the major electrolyte composition of gastric juice at high and low flow rates?

High
- mostly HCL

Low
- interstitial fluid

Is pure oxyntic fluid hyper or hypo osmotic?

Hyper osmotic
(lots of HCL)

Explain the mechanism for generating gastric acid secretion in lumen and the alkaline tide in plasma?

H/K pump = H+ pumped into lumen (stomach)

HCO3 made from cell metabolism goes into plasma via Cl exchanger

Post-Prandial Alkaline Tide

HCO3 made from cell metabolism goes into plasma via Cl exchanger

- causes gastric venous plasma to become alkaline

Why is Cl so important in stomach lumen?

Creates large negative electrical potential on the lumen

- "traps" H+ in lumen
- prevents H+ self attack of mucosa

What 3 molecules stimulate parietal cells and what are there signaling pathways?

1. increase intracellular Ca
- gastrin
- Ach

2. increase cAMP
- histamine

Stimuli for Inter-digestive state

- gastric secretion when at rest

- 15% of maximal

Stimuli for CEPHALIC phase

Thought of meal, smell, taste

Amygdala & Hypothalamus
- low pH of stomach at rest (30% of gastric juice)

1. Dorsal Motor Nucleus
- vagal stimulation releases Ach
- Ach stimulates parietal cell H+ secretion
- Histamine release from ECL cells

2. Postganglionic Parasympathetic Vagus
- GRP released = GASTRIN released from G cells
- inhibits D cells (somatostatin)

Stimuli for GASTRIC phase

Distention of Stomach (50%)

1. vagal-vagal reflex
- food entry neutralizes acid which causes GASTRIN secretion

2. Breakdown products of protein digestion stimulate G-cell directly

Stimuli for intestinal phase

peptides and AA

- activate duodenal G cells to make GASTRIN
- 5%

When is gastric acid secretion maximal?

1 hour after meal ingestion

How does the negative feedback work for acid production?

1. pH falls below 3

2. H+ directly inhibits G cells(most imporant) and parietal cells

3. H+ stimulates D cells (somatostatin)

What are the enterogastrone negative feedback effects on stomach?

1. Secretin
- released in response to acidity in duodenum
- stimulates other release

2. GIP
- stimulus = glucose and fatty acid
- inhibits parietal cells

3. CCK
- stimulus = protein and fat
- reduces stomach motility

Where are the 2 types of pepsinogen from?

1. peptic and mucus cells in parietal glands

2. mucus cells from pyloric glands

How is pepsinogen converted to pepsin?

- at low pH
- pepsin autocatalyzes pepsinogen

What is stimulus for pepsinogen secretion?

1. Ach release from nerve terminals during cephalic and gastric phases of gastric secretion

2. Local acid-sensitive reflex
- vagal input

Duodenal ulcers

- patients have high H+ and pepsinogen secretion

- pepsinogen in plasma

Describe the gastric mucosal barrier.

1. High HCO3 in surface mucus cells = pH7

2. Tight junctions
- prevent back diffusion of H+
-MOST IMPORTANT

What are some agents that disrupt the gastric mucosal barrier?

1. Ethanol
- dissolve lipid membranes
2. Bile salts
3. Drugs (aspirin)
- inhibits PGEs which inhibits acid production (histamine)

Heliobacter Pylori

- gastritis
- peptic ulcer disease
- gastric carcinoma

- causes chronic inflammation
UREASE
- converts urea into ammonia
- buffers H+ = NH4
- destroys mucosal barrier
- MAST cells release histamine = edema= ischemia

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