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chewing
mechanical digestion
fletcher
chew more= more nutrients
saliva
produced by exocrine glands
fluoride, HCO3-, lysozyme
salivary amylase (Carbs)
swallowing
bolus
sphincters
aid but not controlled by gravity
bolus
food and saliva
upper esophagus sphincter
skeletal muscle (voluntary)
Lower esophagus sphincter
smooth (involuntary)
achalasia
high pressure above bolus
lower esophagus sphincter opened
GERD
when lower esophagus sphincter pressure less, stomach acid will come back up
small intestine anatomy
duodenum
jejunum
ileum
vilii
lacteal
duodenum
mixing and digestion
jejunum and ileum
absorption
villi
muscular mucosa layer
receptive relaxation
trigger by food in esophagus
pre emptive
adaptive relaxation
food in stomach
peristalsis (gastric motility)
more in distal stomach
pyloric sphincter is closed
allows for stretching regulated by mechanical stimuli (stretch) and chemical stimuli (digestive product, protein)
proximal portion of stomach
fundus, cardia, body
distal portion of stomach
antrum and pyloric sphincter
proximal stomach function
reservoir
distal stomach function
pumping
very active motility
oblique layer of muscle
rugae
ridges tract stretch on stomach lining
parasympathetic innervation
Ach stimulates secretion of HCl
colonic phase consists of what body parts
large intestine
cecum
colon (ascending, descending, transverse, and sigmoid)
rectum
haustra sacs causes sacs by muscle contraction
mass movements
regulated by meals and circadian rhythm
defeceation reflex
stretch receptors signal smooth muscle contraction
internal anal sphincter
smooth muscle
external anal sphincter
skeletal muscle
dumping syndrome
loss of feedback control
interferes with nutrient digestion
gastric emptying
moving food down from stomach to duodenum
increased tone of gastric reservoir
open/ relax pyloric sphincter (PS)
nervous system innervation needed for this (VIP relaxes PS)
enterogasterones
CCK (fats)
GIP (carbs) > triggers insulin release
secretin (acidity) > brings HCO3- in
when small intestine is active then
pyloric sphincter remains closed
small intestine motility
segmentation > proximal and distal contraction
slow propulsions
infrequent peristalsis
MMC
stimulated by motilin (fasting)
stomach growling
gastric absorption
very little absorption here
alcohol + absorption absorption
restricted by mucus
forms a barrier
chemotherapy targets rapidly dividing cells, including mucosal cells
gastric secretions
LES + pyloric sphincter
mucous + HCO3-
create buffer to protect other tissues
gastric pits
secretory cells are located here
parietal cells
secrete HCl + intrinsic factor for B12 absorption
regulated by protein pump H/K/ ATPase
G cells
secrete gastrin (GQ coupled)
stimulate ECL + parietal cells
ECL cells
secrete histamine (Gs coupled)
stimulates parietal cells
D cells
secrete somatostatin (Gi coupled)
inhibits parietal cells
activated by decrease in pH
chief cells
secrete pepsinogen (inactive)
becomes pepsin when with HCl
G cell activation picture

pancreas exocrine (acinar)
enzymes: amylase, HCO3-, tripisinogen
resulted by enterogasterones
pancreas endocrine
hormones: insulin and glucagon
secretions at duct
acidity stimulates secretin
secretions at acinus
fatty acids
secretions into small intestine
stimulate enzyme release
vagus nerve control
pancreatitis
autodigestion of tissues
liver and gallbladder
produce bile, while stored in gallbladder
made of hepatocytes (liver)
system of ducts connect the two
CCK stimulates bile release from gallbladder
no insulin
hypoglycemic
fasting
post absorptive state
insulin
hyperglycemia
fed
absorptive state
hepatocyte no insulin
glucoginolyis
hexokinase (enzyme)
gluconeogenesis > make new glucose from something else
increase glucose

skeletal muscle/ adipocytes no insulin
glycogenolysis
no glucose 6 phosphate
lipolysis

heptaocyte insulin present
glycogen synthesis
decrease gluconeogensis
decrease glucose

skeletal muscle/ adipocytes insulin
glut 4 at membrane
glycogen synthesis
lipogenesis
