Anatomy and physiology of the GI and hepatobiliary system

Absorption by site - the map that predicts every deficiency

Site	Absorbs
Stomach	Little absorption. Secretes HCl, pepsinogen, intrinsic factor
Duodenum + proximal jejunum	Iron, calcium, magnesium, phosphate, folate, chloride, sulfate
Jejunum	Carbohydrate, protein, water-soluble vitamins - glucose, galactose, fructose, vitamin C, thiamine, riboflavin, pyridoxine
Ileum	Fat-soluble vitamins (ADEK), and in the terminal ileum: bile salts and vitamin B12
Colon	Water, electrolytes, short-chain fatty acids, vitamin K from bacteria

Macronutrient absorption is essentially complete in the upper half of the small intestine - the distal small bowel is functionally redundant for macronutrients in health
- Which is why proximal disease (coeliac) causes iron and folate deficiency, distal disease or resection (Crohn) causes B12 and bile-salt problems, and why short bowel syndrome depends far more on which segment was lost than on how much

Parietal cell - HCl (H+/K+ ATPase, the PPI target) and intrinsic factor
Chief cell - pepsinogen
G cell (antrum) - gastrin
ECL cell - histamine
D cell - somatostatin (inhibitory)
Intrinsic factor binds B12; the complex is absorbed in the TERMINAL ILEUM
- Gastrectomy, pernicious anaemia and terminal ileal disease all end in the same B12 deficiency by different routes

1. Pancreatic lipase + colipase hydrolyse triglycerides -> free fatty acids + monoglycerides

2. Bile acids emulsify them into micelles for enterocyte uptake

3. Enterocyte re-esterifies and packages into chylomicrons

4. Chylomicrons enter LYMPHATICS via the thoracic duct - not the portal vein

*Any of the four steps can fail, and the clinical picture is the same steatorrhoea:*
- Step 1 -> pancreatic insufficiency
- Step 2 -> cholestasis, ileal resection (bile salt loss), SIBO (bile salt deconjugation)
- Step 3 -> abetalipoproteinaemia (no MTP -> no chylomicron assembly)
- Step 4 -> intestinal lymphangiectasia, constrictive pericarditis (high lymphatic pressure)
Medium-chain triglycerides bypass steps 1-4 - absorbed directly into the portal vein without bile or lipase. Hence their use in lymphangiectasia and severe fat malabsorption

<100 cm resected -> bile acids spill into the colon -> bile-salt (choleretic) diarrhoea -> cholestyramine works
- >100 cm resected -> hepatic synthesis cannot keep up -> bile acid deficiency -> steatorrhoea -> cholestyramine makes it worse

Hormone	From	Actions
Gastrin	G cells, antrum	inc acid secretion
Secretin	S cells, duodenum	inc pancreatic bicarbonate, dec gastrin
CCK	I cells, duodenum	Gallbladder contraction, pancreatic enzymes, satiety
GLP-1	L cells, ileum/colon	Incretin, dec gastric emptying, satiety
Motilin	Duodenum	Migrating motor complex (the erythromycin target)
Somatostatin	D cells	Inhibits nearly everything (the octreotide basis)

Function	Test	Note
Synthesis	INR, albumin	INR reflects factor VII - shortest half-life, best acute marker. Albumin half-life ~20 days - chronic only
Excretion	Bilirubin	Not a synthetic marker
Hepatocyte integrity	ALT, AST	ALT more liver-specific; AST also muscle, heart, RBC
Cholestasis	ALP, GGT	GGT confirms a raised ALP is hepatic, not bony
Detoxification	Ammonia	Does not correlate with encephalopathy grade

Carbohydrate buffering: the liver stores excess glucose as glycogen and prevents hypoglycaemia by glycogenolysis and gluconeogenesis
- Hence hypoglycaemia in acute liver failure - and why glucose infusion is standard there
First-pass metabolism: portal blood traverses the liver before the systemic circulation
- Bypassed by portosystemic shunting (cirrhosis, TIPS) -> inc drug levels, inc encephalopathy, and loss of the first-pass advantage of budesonide
Liver also: urea cycle, albumin and clotting factor synthesis, bile acid synthesis, vitamin A/D/B12 storage, iron and copper handling, Kupffer cell clearance of portal endotoxin

B12 stores last 3-5 years; folate stores only 3-4 months - folate deficiency appears far sooner after malabsorption begins
Iron absorption is only ~10% of intake, and is the rate-limiting step in iron balance (there is no regulated route of iron excretion)
Folate deficiency appears in months; B12 deficiency takes years - the same insult produces them at different times
Adaptive hyperplasia of the remaining small bowel after resection continues for 1-2 years - parenteral nutrition can often be weaned during that window
The colon adapts to absorb short-chain fatty acids after small bowel resection - a colon in continuity is worth around 50 cm of small bowel

Gastrectomy or pernicious anaemia -> loss of intrinsic factor -> B12 deficiency; also iron and calcium malabsorption
Terminal ileal resection or Crohn -> B12 deficiency, bile-salt diarrhoea or steatorrhoea, fat-soluble vitamin deficiency, oxalate renal stones (unabsorbed fat binds calcium -> free oxalate absorbed)
Coeliac disease (proximal) -> iron and folate deficiency first; B12 later or not at all
Pancreatic insufficiency -> steatorrhoea + ADEK deficiency, normal mucosa
Bacterial overgrowth -> low B12 (consumed by bacteria) with HIGH folate (produced by them) - the classic discriminating pair
Short bowel syndrome severity depends on: length remaining, presence of the ileocaecal valve, and whether the colon is in continuity

Ileocaecal valve loss -> SIBO and faster transit
Vagotomy -> delayed emptying, dumping syndrome
Roux-en-Y gastric bypass -> iron, B12, calcium, vitamin D, thiamine and copper deficiency
Chronic PPI -> dec B12, dec iron, dec magnesium
Metformin -> B12 malabsorption at the ileal receptor
Cholecystectomy -> continuous low-grade bile flow -> bile-acid diarrhoea

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