pancreas, liver

CCK - released from duodenal I cells when they detect lipids etc, also stimulated to release CCK when LCRF’s (release factors) are not degraded (enzymes acting on chyme instead during digestion) Also Ach (branch of vagus nerve) in response to stomach distension etc intracellular cascade leads to increase Ca2+ levels

S cells produce secretin in response to detecting acid in the duodenum also Ach stimulation leads to increase cAMP and PKA activity increases HCO3/Cl antiporter and activity of CFTR

hepatic artery (nutrients/ oxygenated blood for hepatocytes), hepatic portal vein (venous blood 75% of venous blood from gut flows right through for detoxification) - merge and mix in the sinusoids before draining through the central vein, leaving via the hepatic vein

ECM - produced by stellate cells Stroma protective ECM around liver - strongest at tracts to provide support consists of fibres e.g. collagen, macromolecules and glycoproteins / integrins that link cells to ECM

hydroxyproline produced as a metabolite from stellate cells as they make ECM

cirrhosis / fibrosis, excessive ECM turnover rate leading to higher ECM to cell ratio

lubrication, immune protection (trapping pathogens), mechanical protection, hydration

decreases CCK and secretin release from I and S cells, decreases pancreatic secretions somatostatin analogues can be used clinically e.g. pancreatitis

Hepatocytes, Kupfer cells, biliary epithelium, endothelium, stellate cells

• Form vessels of increasing size to collect canicular bile • Modify content e.g. PH, water • Polarised structure as well e.g. tight adherence to basement membrane to stop damaging bile from secreting into surrounding tissue

• Hepatic resident Macrophages located in the sinusoids • Phagocytosis, regulation of microcirculation (by controlling vascular tone) and removal of endotoxin (part of bacteria cell walls) Can secrete cytokines to illicit a larger immune response, become APC and allow tolerance of favourable molecules e.g. amino acids

• Star shaped with multiple extended membrane processes • In response to disease, can transform into a fibroblast like morphology where they rapidly divide and secrete ECM Perisinusoidal fat / retinoid storing cells

• Squamous epithelial cells that line the vessels of the liver e.g. capillaries • Selective absorption of molecules into the liver, protects from bacteria blood cells etc They also have normal endothelium functions e.g. anti-thrombogenic surface and regulate coagulation and leukocyte activity

• Make up 60-65% of the liver • Polarised epithelial cells • Main functional cell e.g. metabolism, detoxification, bile production Over 100 day life span as they have specialised energy intensive structure

CYP’s levels vary with age, gender, genetics, etc e.g. alcohol abuse = higher levels of CYP540 - problematic for paracetamol overdose CYP may make drugs bioactive or inactive

phase 1 (CYP540) - oxidation / reduction / hydrolysis etc phase 2 - conjugation - makes substance water soluble less toxic for excretion via bile or urine

Jaundice is a yellow appearance of skin, eyes and other tissues due to the buildup of bilirubin, in excess of 2mg/ml

conjugated to albumin as its only lipid soluble

Macrophages (mainly in spleen where rbc are destroyed)

in the liver, its conjugated to guluronic acid by the enzyme UDP glucoronyltransferase it is then conjugated bilirubin

its acted on by bacteria to convert it to urobilinogen

converted to stercobilin (brown pigment) which is excreted in faeces

it is a lipid soluble substance so is bound to albumin and transported back to the liver, where its excreted into bile again as conjugated bilirubin

excreted into bile and to a lesser degree in urine