3. Stomach & Small Intestine Interactions

Stomach – Structure & Mechanical Activity

  • Muscular layers

    • Typical GI tract: circular + longitudinal smooth muscle

    • Stomach adds a third, oblique layer → allows squeeze, shorten AND “wringing/twisting”

  • Sphincters keep contents contained during churning

    • Cardiac (gastro-oesophageal) sphincter – entrance

    • Pyloric sphincter – exit to duodenum

    • Contracted = closed; relaxed = open

  • Time course

    • ~5 h for a normal meal to empty completely into the duodenum

Gastric Juice – Composition, Sources & Purpose

  • Hydrochloric acid (HCl)

    • Extremely low pH  ≈1.5–2\text{pH}\;\approx 1.5–2

    • Kills most microbes

    • Denatures (unfolds) protein → exposes peptide bonds

    • Activates pepsinogen → pepsin

  • Pepsinogen → Pepsin

    • Pepsin = protease initiating protein digestion

    • Secreted by chief cells as inactive “-ogen” for self-protection

  • Gastric lipase – minor fat digestion

  • Intrinsic factor (IF)

    • Required later (ileum/colon) for vitamin B12\text{vitamin B}_{12} absorption → essential for erythropoiesis

  • Mucus

    • Thick, viscous, alkaline (high pH\text{pH})

    • Produced by surface goblet cells → coats epithelium, buffers acid, lubricates rough chyme

Self-Protection Strategies of the Stomach

  • Goblet‐cell mucus barrier (thick + alkaline)

  • Proteolytic enzymes secreted as inactive zymogens (eg. pepsinogen)

  • Acid/enzymes only released when food is anticipated or present (regulated secretion)

Regulation of Gastric Function – Three Phases

  • Cephalic phase (“head”)

    • Trigger: sight/smell/thought of food

    • Parasympathetic (vagus) ↑ acid, enzyme, mucus secretion & mild motility (stomach “rumbling”)

  • Gastric phase (“stomach”)

    • Trigger: food distension & partly digested peptides

    • Local ENS reflexes + hormone gastrin (from G-cells) ↑↑ secretion & strong mixing waves

  • Intestinal phase (“small intestine”)

    • Trigger: chyme enters duodenum (low pH\text{pH}, hypertonic, fatty acids, amino acids, stretch)

    • Duodenal hormones:

    • Secretin → ↓ gastric motility/secretion; ↑ pancreatic HCO3−\text{HCO}_{3}^{-}

    • CCK (cholecystokinin) → ↓ gastric activity; ↑ pancreatic enzymes & bile release

    • Enterogastric reflex (neural) reinforces inhibition

Why Is Chyme Released Slowly?

  • Chyme features: low pH\text{pH}, hypertonic, partially digested nutrients

  • Small intestine tasks = finish digestion + absorb

  • Too large a bolus would:

    • Overwhelm enzyme supply → incomplete digestion/absorption

    • Create major osmotic pull → water shifts from blood → lumen → ↓ blood volume, hypotension, rapid transit

    • Deliver excessive acid → mucosal injury (needs buffering to pH≈8\text{pH}\approx 8)

Small Intestine – Anatomy & Functions

  • Regions (proximal → distal)

    1. Duodenum (~25 cm) – finishes chemical digestion

    2. Jejunum (~2.5 m) – bulk nutrient absorption

    3. Ileum (~3.5 m) – remaining absorption; bile salts & B12\text{B}_{12}–IF complex

  • Total length ≈ 5–6 m, yet internal surface ≈ tennis-court sized due to folds

Accessory Organ Inputs

  • Liver → bile production

  • Gallbladder → bile concentration & storage; contracts when signalled

  • Pancreas (99 % exocrine) → pancreatic juice

    • HCO3−\text{HCO}_{3}^{-} to neutralise acid

    • Enzymes: amylase (carbs), lipase (fats), protease zymogens (trypsinogen, chymotrypsinogen, etc.), nucleases

  • Sphincter of Oddi (hepatopancreatic ampulla) regulates common entry into duodenum

Zymogen Activation Cascade in the Duodenum

  • Pancreatic acinar cells release inactive enzymes

  • Brush-border enterokinase on mucosal microvilli:

    1. Activates trypsinogen → trypsin

    2. Trypsin then activates chymotrypsinogen & other pro-proteases

  • Protection rationale: prevents autodigestion of pancreatic & ductal tissues

Bile – Composition & Role

  • Made in hepatocytes, stored in gallbladder

  • Constituents

    • Bile salts (derived from cholesterol) – amphipathic

    • Bilirubin (heme breakdown product) – excretory pigment

    • Cholesterol, phospholipids, electrolytes, water

  • Function: emulsification (NOT hydrolysis) of dietary fat

    • Breaks large lipid globules → many small droplets → ↑ surface area for pancreatic lipase

Hormonal Coordination of Duodenal Events

  • Stimulus: chyme (fatty acids + amino acids, low pH\text{pH})

  • CCK (red dots in diagram)

    • Source: duodenal I-cells

    • Targets & actions

    • Pancreas → enzyme-rich juice

    • Gallbladder → contraction

    • Liver → ↑ bile production

    • Sphincter of Oddi → relaxation

    • Stomach → ↓ motility & secretion

  • Secretin (yellow dots)

    • Source: duodenal S-cells (respond to acid)

    • Actions

    • Pancreas → bicarbonate-rich juice

    • Liver → synergises with CCK for bile flow

    • Stomach → ↓ acid output & motility

Intestinal Motility Patterns

  • Segmentation (localized circular contractions)

    • Mixes chyme with enzymes, exposes it to mucosa, slow propulsion

  • Peristalsis (longitudinal wave)

    • After most absorption or when new meal arrives -> clears chyme toward colon

Mucosal Adaptations for Absorption

  • Circular folds (plicae circulares) – large ridges ↑ area ×3

  • Villi – finger-like projections ↑ area ×10

    • Each villus contains

    • Capillary network → carries monosaccharides & amino acids to liver via portal vein

    • Lacteal (lymphatic capillary) → absorbs lipid-rich chylomicrons

  • Microvilli (“brush border”) on enterocyte apical membrane ↑ area ×20 & house brush-border enzymes incl. enterokinase

  • Peyer’s patches (ileum) – aggregated lymphoid nodules → immune surveillance

Mechanisms of Nutrient Uptake

Carbohydrates

  • Glucose and galactose are absorbed into intestinal cells through SGLT1, which is a sodium-dependent (Na⁺) secondary active transporter.

  • Fructose is absorbed via GLUT5, using facilitated diffusion, which does not require energy.

Proteins

  • Amino acids and small peptides are absorbed using Na⁺-coupled transport and H⁺/peptide cotransporters.

Lipids

  • Fatty acids and monoglycerides are carried to the intestinal wall by bile salt micelles, then absorbed via simple diffusion into the cell.

  • Inside the cell, they are re-formed into triglycerides, packaged into chylomicrons, and released by exocytosis into the lacteal (lymph capillary).

  • From the lacteal, they travel through the thoracic duct and enter the bloodstream.

Water

  • Water moves by osmosis, following the movement of absorbed solutes.

  • If the intestinal contents (chyme) are still hypertonic, water may flow back into the lumen, causing dehydration and diarrhoea.

Clinical / Physiological Implications & Connections

  • Gastrectomy (removal of the stomach) or chronic gastritis can reduce or stop the production of intrinsic factor (IF), leading to vitamin B₁₂ deficiency and pernicious anaemia.

  • Rapid gastric emptying (also called dumping syndrome) can cause low blood pressure, diarrhoea, and poor nutrient absorption due to fluid being drawn into the gut too quickly.

  • Pancreatitis risk increases if digestive enzymes (zymogens) are activated too early inside the pancreas, damaging tissue.

  • Digestive organs are interdependent:

    • Stomach damage not only affects digestion but also stops IF production.

    • Duodenum damage can impair hormones like CCK and secretin, leading to uncontrolled stomach activity.

  • The parasympathetic nervous system (rest-and-digest) stimulates digestion, while the sympathetic nervous system (fight-or-flight) slows it down. This links stress, digestion, and energy balance.