Digestive System – Accessory Organs & Large Intestine Vocabulary

Pancreas – Dual Roles

• Accessory organ that “taps” into the GI tube at the duodenum via the major duodenal papilla (described as a tiny “belly-button”).
• Two distinct functions
  • Endocrine: glucose regulation (insulin, glucagon) directly into bloodstream.
  • Exocrine: secretion of pancreatic juice through the pancreatic duct.
  • Composition & purpose
    • Alkaline bicarbonate‐rich buffers neutralize gastric \text{HCl}. Classic reaction: \text{HCl}+\text{NaHCO3}\;\longrightarrow\;\text{NaCl}+\text{H2O}+\text{CO_2}.
    • Digestive enzymes
    • Amylases → polysaccharides → disaccharides/monosaccharides.
    • Proteases → proteins → peptides/amino acids.
    • Lipases → triglycerides → fatty acids + glycerol.
• Merges with the common bile duct (liver + gallbladder) just before entering the duodenum.

Liver – Anatomy, Histology & Massive Function List

• Performs ≈ 200 (probably more) separate functions; highlights:
  • Detoxifies blood (drugs, alcohol, hormones, antibodies, pathogens).
  • Carbohydrate, lipid & amino-acid metabolism (both anabolic & catabolic; e.g., glycogen ↔ glucose).
  • Synthesizes plasma proteins, many clotting factors.
  • Stores fat-soluble vitamins A,D,E,K; converts vitamin D_3 → precursor for renal calcitriol (Ca^{2+} absorption).
  • Produces bile (critical for fat emulsification).
• Remarkable regeneration: surgical removal triggers growth back to original size & shape—not a “cauliflower” deformity.
• External features
  • Encased in a capsule; right lobe larger, left lobe smaller, separated by falciform ligament.
  • Large right lobe slightly displaces right kidney inferiorly.
• Internal micro-architecture
  • Consists of lobes → lobules (hexagonal “vats”).
  • Parenchyma made of hepatocytes.
  • Three intertwined tube systems
  1. Hepatic artery (red) – oxygen-rich arterial blood.
  2. Hepatic portal vein (blue) – nutrient-rich venous return directly from small intestine.
  3. Bile canaliculi (green) – carry freshly made bile to bile ducts.
  • Sinusoids = cavernous, fenestrated capillaries where portal blood percolates; site of nutrient “tweaking.”
• Bile action once in duodenum
  • Emulsification = breaks large fat globules → many tiny droplets, ↑ surface area for pancreatic lipase.

Hepatic Portal System – Specialized Circulation

• Venous mesh drains stomach, small & large intestines → joins to form the singular hepatic portal vein.
• Vein enters the inferior surface of liver, then ramifies into sinusoids; blood finally reaches the inferior vena cava only after traversing liver tissue.
• Functional sequence
  1. Absorption in small intestine.
  2. Immediate delivery to liver for first-pass processing (add/remove sugars, lipids, toxins, water, etc.).
  3. Modified blood exits via hepatic veins → inferior vena cava → systemic circulation.

Gallbladder – Storage, Not Manufacture

• Small green sac nestled on liver’s inferior surface.
• Stores & concentrates bile; ejects via cystic duct → common bile duct → duodenum.
• Clinical issues
  • Gallstones (cholelithiasis) → inflamed gallbladder (cholecystitis); X-ray or ultrasound shows stones; often surgically removed.
  • Clogged bile duct may back-up bilirubin → jaundice.
  • Evolutionary aside: removal common but biologist’s caution re: losing a once-useful organ.

Liver & Biliary Pathologies

• Hepatitis = inflammation of liver.
  • Viral: Hep-A, B, C, D, E, F, G… Acute or chronic.
  • Alcoholic hepatitis – ethanol-induced.
• Cirrhosis = progressive, irreversible scarring; loss of functional hepatocytes.

Large Intestine – Macro-Anatomy & Transit

• Primary roles: water reclamation, vitamin & bile-salt absorption, fecal storage.
  • Water volume may drop from 1500\;\text{mL} → 200\;\text{mL}.
• Segments (cecum → colon → rectum → anus)
  1. Cecum – blind pouch; meeting of ileum; bears the vermiform appendix.
  • Appendage may reseed gut flora; analogous to very large cecum of herbivores (e.g., rabbits).
  1. Ascending, transverse, descending colon.
  2. Sigmoid colon – S-shaped curve leading to rectum.
  3. Rectum & anal canal.
• Special features
  • Haustra – pocket-like pouches allow expansion/elongation.
  • Teniae coli – longitudinal ribbon of muscle creating the haustral segmentation.
• Motility & reflexes
  • Powerful peristalsis in upper GI; distension of rectum triggers defecation reflex.
  • Sphincters
  • Internal anal sphincter – smooth muscle, involuntary.
  • External anal sphincter – skeletal muscle, learned voluntary control (potty training parallel to external urethral sphincter).
  • Hemorrhoids – varicosities of anal veins (internal/external); may bleed & hurt.

Histology of the Large Intestine

• Thin mucosal wall, deep intestinal glands (crypts) but no villi (little nutrient absorption).
• Abundant goblet cells → mucus for lubrication.
• Diverticulosis – formation of mucosal pockets; when inflamed → diverticulitis (pain, altered bowel habits). Old seed-lodging theory now questioned.

Gut Microbiota – “Second Brain”

• Population size ≈ 10^{14} microbes from \sim thousands of species; microbial cells outnumber host colonic cells dramatically.
• Interaction spectrum
  • Mutualism ↔ Commensalism? ↔ Parasitism – dynamic & host-health–dependent.
  • Example species
  • Potentially helpful: Enterococcus, Bifidobacterium, Lactobacillus.
  • Context-dependent: E. coli (harmless in colon, pathogenic elsewhere).
  • Clearly pathogenic: Clostridium difficile, Campylobacter.
• Clinical/physiological significance
  • Implicated in metabolic regulation (diabetes), mood & cognition, pain/fatigue syndromes.
  • Communicate via quorum sensing (chemical “census”).
• Modulation strategies
  • Yogurt/probiotics–must contain “live & active cultures” & survive stomach acid; watch for high added sugar.
  • Antibiotics, diet, immune status can shift balance (e.g., C. difficile overgrowth post-antibiotics).
• Immune landscape
  • Dense population of resident immune cells patrol mucosa—constant monitoring of this “external” environment.

Food Poisoning – Timing & Tracing

• Symptom‐onset window provides pathogen clues
  • Pre-formed toxin ingested → symptoms within \text{~2–6 h} (e.g., Staphylococcus aureus enterotoxin).
  • Bacteria must synthesize toxin in host → \text{~8–96 h} latency.
  • Protozoa or other longer-cycling organisms → days to weeks.
• Detective work: epidemiologists track common dining sites/products (example outbreaks: salmonella in peanut butter, spinach, cucumbers; Kinder Surprise eggs).
• Practical takeaway: stringent food-handling & kitchen hygiene—no food group is automatically “safe.”

Quick Disease & Disorder Reference

• Cholecystitis – gallbladder inflammation from stones.
• Jaundice – bilirubin accumulation (e.g., bile duct obstruction).
• Diverticulitis – inflamed diverticula (LLQ pain, fever).
• Hemorrhoids – venous varicosities.
• Cirrhosis – irreversible hepatic fibrosis.

Course/Lab & Study Reminders

• This lecture completes Digestion Module 3; be sure laboratory modules & exercises are also up-to-date.
• Finish the Digestion quiz before attempting Test 3.
• Instructor encouragement: acknowledge your progress, reach out with questions, and continue diligent A&P study!