- Gastrointestinal Physiology
- metabolism
- starvation
- 24 hours
- reduced RQ
- increased glycogenolysis (stores last for 24 hrs)
- increased urinary nitrogen as amino acids are deaminated for gluconeogenesis
- 24-72 hours
- ketogenesis
- heart and brain use ketones
- metabolic acidosis
- start of lipolysis and proteolysis
- >72 hours
- ketones main source of energy for the brain
- further lipolysis and proteolysis
- ketoadaptation begins and gluconeogenesis decreases
- glucose
- hormones
- glucagon
- 29 amino acids, single chain
- acts on liver by GPCR’s
- secreted by alpha cells
- insulin
- 51 amino acids, double chain with 2 disulphide bridges
- 5600 Da
- acts via tyrosine kinase receptors to translocate glucose transporters to the cell membrane
- secreted by beta cells
- brain, red cells and adrenal medulla can ONLY use glucose as a substrate
- BMR
- for every 1 degree temperature increase/decrease, cerebral metabolic rate increases/decreases by 5-8%,
- must be measured 12-14hrs after last meal
- absorption
- Stomach
- phases
- cephalic
- 3 mechanisms
- vagal impulses activate Ach receptors on parietal cells and stimulate HCl secretion
- H/K ATPase (proton pump) pumps H into stomach
- HCO3- exchanged for Cl- on basolateral membrane —> passively move into stomach
- PPI’s inhibit this
- can produce complete achlorhydria
- vagal impulses activate Ach receptors on G ells and stimulate gastrin secretion, which also stimulates parietal HCl secretion
- In Zollinger-Ellison syndrome, a tumour of the pancreas/duodenum/lymph nodes secretes gastrin
- vagal impulses and gastrin stimulate histamine release from mast cells, which increase HCl secretion
- H2 antagonists (ranitidine) inhibit this
- gastric
- peptides, amino acids and a raised pH stimulate HCl secretion
- mechanoreceptors in stomach are stretched and increase vagal stimulation
- intestinal
- when duodenum becomes distended
- fatty acids and low pH in duodenum stimulate secretin release
- inhbits gastrin secretion
- fatty acids stimulate gasric inhibitory peptide and cholecytokinin
- inhibit gastrin and HCl secretion
- VIPoma
- vasoactive intestinal polypeptide
- often part of MEN-1
- inhibits gastric acid and causes secretion of large amounts of water and electrolytes into the intestine
- not all bad
- also doubles vaginal lubrication
- liver
- function ‘EMI’
- exocrine
- bile
- digests and absorbs fats
- neutralises gastric acid
- excretes bilirubin and cholesterol
- metabolic (anabolism and catabolism)
- drugs
- protein
- fat
- carbohydrate
- immune
- high levels of macrophages and lymphocytes
- blood supply
- 25% of CO = 1.25L/min
- hepatic artery
- 1/3
- control of flow
- intrinsic
- adenosine causes vasodilation in response to low PV flow (hepatic artery buffering)
- myogenic autoregulation
- extrinsic
- alpha and beta adrenoceptors
- circulating factors
- angiotensin, endothelin, vasopressin, glucagon, histamine
- portal vein
- 2/3
- sats 85% (less after eating)
- control of flow
- extrinsic only
- only alpha adrenoceptors
- ciculating factors
- structure
- lobule
- 1-2mm diameter
- components
- peripheral portal triad
- bile ductile
- bile cannaliculi merge to form these ductiles
- hepatic artery branch
- portal vein branch
- plus more recently discovered!
- lymphatic vessels
- branch of vagus nerve
- central vein
- sinusoids
- capillaries between hepatocytes
- contain Kuppfer cells (specialised macrophages)
- hepatocytes
- periportal
- best oxygen supply
- so most metabolically active
- gluconeogenesis
- beta-oxidation of fatty acids
- cholesterol synthesis
- but most susceptible to viral hepatitis
- centrilobular
- poor oxygen supply
- most P450
- glycolysis
- lipogenesis
- most susceptible to (centrilobar) necrosis