PNB 2265 Exam 3

spring 2026

Functions of GI Tract

Ingestion of nutrients, secretion, mechanical & chemical processing, absorption, excretion

sphincter muscles

keep different regions of tube physically & functionally separate, smooth muscle, doing primarily tonic (sustained) contraction

Parietal peritoneum

Lines walls of abdominal cavity

Visceral peritoneum

Covers the surface of the organs

Greater omentum

Covers most of the ventral surface of the abdomen; stores a lot of adipose tissue

Serosa

outermost tissue layer, connective tissue wrapper

Muscularis

second outermost, muscle & nervous tissue layer that creates motility, longitudinal and circular layers

Submucosa

second innermost layer, nervous & connective & lympathic, binds things together

Mucosa

innermost layer, muscle & nervous & lymphatic & epithelial

3 sublayers: muscularis mucosae (shape folds), lamina propria (lymph nodes, WBC, protect from pathogens), epithelium (enterocytes, enteroendocrine, mucin-producing cells, gastric pits)

Myenteric plexus

inside nervous tissue layer between circular and longitudinal muscularis layers, major site of GI tract innervation. myo = muscles, controls smooth muscle of GI tract wall

Peristalsis

forward movement, high pressure behind food and low pressure in front of food (proximal contraction & distal relaxation), occurs in antrum (mostly distal stomach)

Segmentation

back and forth movements

Phasic contractions

acute (quick) contractions, present throughout GI tract, produce movements

Tonic contractions

sustained (long) contractions, sphincter muscles, prevent backflow

Small intestine

major site of digestion & absorption

Cephalic phase

head, chewing, salivary amylase & lipase, lysozyme, fluoride, HCO3-, secreted by parotid, sublingual, & submandibular glands in autonomic regulation

Gastrointestinal Reflux

Failure of lower esophageal sphincter to close properly, leading to stomach acid moving up, increase in gastric pressure or decrease in esophageal pressure

Esophageal pressure is reduced by

Caffeine, alcohol, cigarettes, chocolate

Rugae

increase surface area of stomach, stretch as stomach increases in volume

Oblique layer

Layer of muscle present on muscularis externa, more muscle = more contraction

Chief cells

secrete pepsinogen

Mucus cells

secrete mucus

G-cells

secrete gastrin hormone

D cells

secrete the peptide messenger somatostatin —> decreasing acid production

Enterochromaffin-like cells (ECL)

secrete histamine

Endopeptidases

start in stomach, cut polypeptide chains somewhere in the center, creating many small peptide fragments, stomach (pepsin) or pancreatic (trypsin) secretions

Exopeptidases

start in intestine, release single amino acids, pancreas (ex. carboxypeptidase)

Amino acids are transported by

Na+ symporters

Di/Tripeptides are transported by

H+ symport

Large peptides ex. antibodies are transported by

endocytosis

Fat digestion

Mechanically broken up, coated in bile which makes the surface water-soluble, attacked by water-soluble lipases from pancreas, convert into monoglycerides & free fatty acids, perform into micelle which is then absorbed via diffusion, gets packaged into chylomicron which then goes into lacteal and passes through entire lymphatic system

Hepatic portal system

Venous blood from gut → hepatic portal vein → liver metabolism: carbs, amino acids, lipids, detoxification → drains through hepatic vein (to vena cava)

Alcohol detoxification

Alcohol dehydrogenase turns ethanol into acetaldehyde, toxic intermediate, then acetaldehyde dehydrogenase converts acetaldehyde into acetic acid using glutathione as cofactor

Alcohol flush syndrome

overactive alcohol dehydrogenase enzyme present in just under half of East Asian population

Achalasia

caused by muscle contraction/high pressure in lower esophagus, so bolus cannot move

Histamine

locally released in gastric pit by ECL cells, has receptors on basolateral membrane of parietal cell that is Gs coupled, triggers release of cAMP which activates protein kinase A

Protein Kinase A

cAMP-dependent, phosphorylates proton pump → increases acid production

Protein Kinase C

Calcium-dependent, phosphorylates proton pump → increases acid production

Acetylcholine & Gastrin

receptors are Gq-coupled, trigger release in intracellular Ca2+

Somatostatin/PGE₂

Gi-coupled, inhibits cAMP, inhibits protein kinase A activation → decreases acid production

Receptive relaxation

as bolus passes down esophagus, activates stretch receptors & triggers relaxation in stomach, pre-emptive

Adaptive relaxation

once you have the food in your stomach, the walls themselves stretch

Enterogastrones

gastrointestinal hormones (ex. secretin, CCK, GIP) inhibiting gastric secretion and stomach motility

Secretin

inhibitory to gastric secretion, stimulated by decrease in pH, bring bicarbonate into small intestine to neutralize stomach acid

Cholecystokinin (CCK)

triggers gallbladder to release bile, stimulates pancreas to secrete digestive enzymes, delays gastric emptying (stimulates feeling of satiety), released in response to increase in fats

Gastric inhibitory peptide (GIP)

slow stomach emptying, released in response to an increase in carbohydrates

Hepatic duct

to gallbladder

Common bile duct

to duodenum

Pancreatic Acini (Acinus)

exocrine, made up of bulb (salivary amylase) connecting to duct (bicarbonate), precursors (trypsinogen, chymotrypsinogen, procarboxypeptidase)

Pancreatic Islet

endocrine, hormones

Dumping syndrome

Stomach prematurely dumps contents into duodenum, loss of feedback control, pain/cramping/malabsorption

Migrating Motor Complex (MMC)

stimulation of peristalsis in response to fasting using hormones like motilin, inhibition during feeding

Arcuate Nucleus

region of hypothalamus with anorexigenic and orexigenic neurons

Anorexigenic neurons

stimulates neurons in paraventricular nuclei → satiety

Vagus stimulation

afferent, distension (stretching) of gut

Anorexigenic hormones/peptides

Small intestine: CCK, GIP, secretin

Gut nervous system: VIP

Pancreas: insulin

Adipose tissue: leptin (inhibits orexigenic neurons)

Orexigenic hormones

Stomach: ghrelin

Zymogens

inactive enzymes released by pancreas that must be activated in lumen → need for activation prevents autodigestion of our own tissues

Pancreatitis

autodigestion of pancreas

Hepatocytes

cells that make up liver, produce bile

Hepatic duct

to liver, connects to common bile duct

Cystic duct

connects to gallbladder

Pancreatic duct

connects to pancreas, secrete bicarbonate (HCO₃)

Neuropeptide Y (NPY)

inhibits satiety, increases in response to stress, thought to contribute to stress eating

Cholesterol

critical component of plasma membrane, contributing factor to atherosclerosis, is incorporated into bile by liver, is incorporated into steroid hormones by cortical cells

Lipostatic Theory

signals from fat modulate eating behavior, metabolism adjusts based on amount of fat body produces

Leptin

“obesity gene,” secreted by adipocytes, inhibits orexigenic receptors → promotes satiety, adjusts metabolism in peripheral tissues

Glucostatic Theory

Metabolism adjusts to maintain homeostatic level of glucose

Fed (Absorptive) State

of glucostatic theory, hyperglycemic (high glucose), activate storage processes, increased synthesis

Fasted (Post-Absorptive) State

of glucostatic theory, hypoglycemic (low glucose), increased catabolism and access to stored energy

Gluconeogenesis

making glucose from non-carbohydrate sources

Glycogen

complex, highly branched carbohydrate polymer made up of glucose molecules, easily and quickly made via glycogenesis, short-term storage, stored in liver and skeletal muscle

Triglycerides

higher energy content, little water is required for fat storage, harder & slower to access, excess glucose leads to fat production via lipogenesis, long-term storage molecule, need to be digested by lipoprotein lipase (LPL) to move into adipocyte

Glycogen Synthase

in skeletal/liver tissue, catalyze formation of glycosidic bond (rate-limiting step) of turning glucose into glycogen

Glycogen Phosphorylase

kinase that phosphorylates glycogen and causes dissociation of glucose subunits into glucose phosphate monomers (glucose-1-phosphate → glucose-6-phosphate

Glucose-6-Phosphatase

Remove phosphate (dephosphorylation) of G-6-phosphate to form glucose, skeletal muscle does not have

Protein

cannot be stored in body, must be used by cells or broken down via gluconeogenesis; some amino acids can be converted to pyruvate

Beta Oxidation

free fatty acids used by most cells for fuel, can be used for acetyl-CoA formation

Hormone Sensitive Lipase

break down triglycerides stored in adipocytes into glycerol and fatty acids

Chylomicrons

fat components and cholesterol from bile & proteins, exocytosed across basal lateral membrane to lacteals and pass through lymphatic system

Very Low Density Lipoprotein (VLDL)

very high fat & cholesterol %, made in liver from chylomicrons, ApoB/C

Low Density Lipoprotein (LDL)

higher % cholesterol than protein, delivers cholesterol to tissues, formed from VLDL in circulation, ApoB/C

High Density Lipoprotein (HDL)

high % protein to cholesterol, made primarily in liver then small intestine, accepts cholesterol and transports it to liver, ApoA

Scavenger receptor (SCARB)

liver and cortical cells, allows liver to get cholesterol and convert it into bile, allows cortical cells to synthesize steroid hormones

Atherosclerosis

accumulation of cholesterol in circulation and attach to walls of blood vessels → formation of plaques, HDL:LDL ratio is most predictive as LDL increases as we age which significantly increases cardiovascular disease risk