lead into the liver
hepatic artery and hepatic portal vein
lead out of the liver
hepatic veins and common hepatic duct
be able to label the following on lobules
central vein, branch of hepatic artery, branch of portal vein
big canal between hepatocyte cords
sinusoid
small canal between hepatocyte cords
bile canaliculus
modify the blood in the liver by adding or removing certain materials
hepatocytes
special about liver, gives it direct access to blood
no endothelial layer
can activate or inactivate drugs/chemicals in the liver
CYP enzymes
additions/subtractions that CYP can do
hydroxylation, dealkylation, deamination, hydrolysis
drugs that cannot be taken with grapefruit due to effect on CYP enzymes
Xanax, Lipitor, Allegra
causes of variation in CYP affectiveness
genetics, liver failure due to age, alcoholism, or hepatitis
phagocytes in the liver that remove foreign objects from the blood
Kupffer cells
things placed in bile
cholesterol, bilirubin, HCO3-, water, bile salts
where bile is stored
gallbladder
be able to label the following organs and ducts involving bile
liver, common hepatic duct, common bile duct, pancreas, cystic duct, sphincter of oddi, pancreatic duct, duodenum
how bile is let into the duodenum
the sphincter of oddi relaxes during eating periods to let it through
what amount bile must be concentrated down to
50mL/12hr
actively transported out of bile, followed by water
Na+
become more concentrated in bile after sodium and water leave
bile salts, HCO3-, bilirubin, and cholesterol
can form gallstones
bilirubin and cholesterol
symptoms gallstones can cause
poor digestion, jaundice, pain, toxicity, inflammation
contractions of these cause bile to be released into the duodenum
CCK stimulates gallbladder contraction, sphincter relaxes
neutralizes acid in duodenum
HCO3-
how bile salts emulsify fats
attaches to them to form a micelle, which can be absorbed into the blood stream
steatorrhea
fats in feces from lack of absorption
stimulates islets for insulin secretion
incretin
bicarbonate cycle
liver-->gallbladder-->duodenum-->blood-->liver again
breakdown of proteins
into amino acids by pepsin and trypsin
breakdown of carbohydrates
into sugars by amylase
breakdown of nucleic acids
into nucleotides by nucleases
breakdown of fats
into fatty acids by lipases
3 step process of absorption
get into cytoplasm, get it to cross other side of cell, get it into blood or lymph
modifications that maximize intestinal absorption
circular folds, villi, and microvilli
absorption of sugar
cotransport with sodium, sodium is actively transported out
absorption of fatty acids
micelles detach their phospholipids, which use flippases to flip across the bilayer and form into triglycerol
protein coated micelles
chylomicron
absorption of amino acids
can be absorbed in singles, pairs, or triplets, energy is from Na+ or H+ concentration gradient
absorption of electrolytes
Positive ions use facilitated diffusion, negative ions use positive ions, water uses osmosis, potassium uses concentration gradient
stimulates Na+ absorption
aldosterone
stimulates Ca+2 absorption
PTH
amount of fluid reabsorbed and added to digestive system
7 liters
amount of fluid that must be consumed to avoid dehydration
2 liters
types of ulcers
gastric and duodenal
what ulcers are
erosions in the mucus membrane, exposed directly to stomach acid
bacteria that causes ulcers
H. pylori
hormones that stimulate proton potassium ATPase pump
gastrin, ACh, histamine
bleeding ulcer
basement membrane broke and allowed blood in
treatments for ulcers
antibiotics and proton pump inhibitors, histamine receptor antagonists, prostaglandin E1 analog, antacids
why NSAIDs are counterproductive in ulcers
they inhibit prostaglandin production
celiac disease
undigested gluten gets through villi into ISF, humoral immune system responds, neutrophils lyse and cause damage