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114 Cards in this Set

  • Front
  • Back
VIP (vasoactive intestinal peptide)
made in the small intestine
released when chyme/fat enters pH change or stretch in the stomach
vasodialation stims HCO3 mucous making (alkaline)
made in the stomach
released bc of stretch or pH Change
stim enzyme release, relaxes sphincters, mass movement, contraction of stomach and small intestines
GIP (gastric inhibitory peptide)
made in the small intestine
released bc fat/chyme in small intestine, stomach stretch, pH change
CCK (Cholecystokin)
made in the small intestines
released bc fat/chyme in the small intestines , stomach stretch, pH change
inhibits stomach, stim pancreas enzymes, relaxes sphincters
made in the small intestine
released bc chyme/fat in small intestine, stretch of the stomach, pH change
inhibits secretions of the stomach, stim bile production, stim HCO3 secretion in the pancreas
Brush-border sucrase
breaks down sucrose to (fructose and glucose)
found in the small intestine
Brush-Border maltase
breaks down maltose into 2 glucoses
found in the small intestine
Brush-Border lactose
breaks down lactose into glucose and glactose
found in the small intestine
Pancreatic lipase
made in the pancreas
CCK stims this release
breaks down lipids
in the stomach
released inactively as pepsinogen (activated by HCl)
breaks down peptides/protiens
Salivary Amaylase
found in the mouth from the salivary glands
released in reaction to startch in the mouth breaks it down
Pancreatic Amylase
made in the pancreas
CCK stims this release
breaks down starches in the small intestines
released inactive as Trypsinogen
activates chymotrypsinogen and procarboxypeptidase
made in the pancreas
breaks down protien chains
inactive form chymotrypsinogen
made in the pancreas
breaks down protiens cuts the chain where ever
procarboxypeptidase inactive form
made in the pancreas
breaks down protiens by starting with the acid side breaks of one aminoacid at a time
found in the lining of the small intestine
activates Trypsinogen into Trypsin
intestinal Lipase
brush-border enzyme in the small intestine
breaks down fats into fatty acids and gylcerol
sum of all the chemical processes occurring in the body
reactions in which larger molecules manufactured from smaller ones
require energy (ATP) input
reactions in which larger molecules are broken into smaller ones
Trigylcerides break into?
3 fatty acids and a gylcerol
GLycogen breaks into?
Protiens breaks into ??
Aminoacids break into?
amine group and keto acid
Significance of nutrient pool and Kreb's/ TCA cycle
Nutrient pool (small carbon chains) go into the Kreb's cycle generating 36 ATP and CO2 waste and co-enzmyes which enter the electron transport chain to yield crap loads of ATP and H2O (bc H is the final acceptor)
chemical formula for glucose oxidation
C6H12O6 + 6 O2  6 CO2 + 6 H2O
Breakdown of glucose to produce ATP
Synthesis of glucose from noncarbohydrate precursors
only in the liver!!!
Formation of glycogen
Breakdown of glycogen
Role of the liver in metabolism
Carbohydrate metabolism
Stores glucose as glycogen (long, branching chains of glucose) by glycogenesis
breaks down glycogen (glycogenolysis) to release glucose to maintain blood glucose levels
trygylcerides(lipids) are broken into 3 fatty acid chains and one gylcerol
Fatty acid molecules broken into Acetyl CO-A (2 carbon molecules)
generate alot of ATP but very slowly
occurs in the liver
2 acetyl-CoA -> acetoacetic acid -> ketones i.e.beta-hydroxybutyric acid or acetone
mesentery proper
around the small intestines anchors the organs to the back of the abdominal cavity for bd vessels nutrients and nerves
lesser omentum
superior to the stomach run inferior of the liver
connects the vessels into the hepatic portal system
greater omentum
inferior of the stomnach down anterior of he cavity back up connects to the transverse colon
peritoneal ligaments
small mesentery falciform connects liver to the diaphragm
intraperiptneal cavity -> visceral layer surrounds the organ and the cavity
retroperiotneal --> organ in the cavity is surrounded by/behind 2 layers less protection more seclusion this is a mesentery
rythmic contractio of the tube's circular muscles alternately in the stomach and small intestine
peristaltis -> ring of contraction (proximal pinch) longitudinal contraction (squish food distally)
the 6 sphincters
hypopharyngeal (btwn pharynx and esophagous)
gastro-esophageal (btwn esophagous and stomach (around T11))
pyloric sphincter (stomach to the small intestine)
illeo-cecal valve ( btwn illeum and cecum )
internal anal sphincter (smooth muslce)
exturnal anal sphincter (skelatal muscle)
Small intestine
90% of digestion
Plicae circulares
circular folds mucousal and submusousal layers
greater surface area causes chyme to move in a circular motion
goblet cells
found in the gastric pits and the small intestine folds secretes a protective mucous in both places
Enteroendocrine cells
also secretes mucous in the small intestine
intestinal glands/ cyrpts
Secrete intestinal juice mucous,bicarbonate, water, electrolytes for absorbing

Paneth cells secrete lysozyme

Duodenum glands secretes even more cells
Migrating myoelectric complex (MMC)
Move only a couple of inches to slow down the movement of chyme
Weak peristalsis in comparison to the stomach
chyme remains for 3 to 5 hours
Moves undigested chyme to large intestine
local mixing of chyme with intestinal juices---sloshing back & forth
Mechanical digestion
Force can be altered by hormones, enteric, ANS bc it is always going on
enteric reflex
Distension (stretch) of duodenum initiates segmentation
gastroileal reflex
increased stomach activity intiates this reflex
long reflex involving brain and parasympathetic innervation (enhances force of segmentation in ileum) relaxes the valve
mechanical digestion (in the small intestine)
bile salts secreted by liver (stored in and released from gall bladder) emulsify fat globules (make them into smaller droplets) to increase surface area lipases have available to work on (emulsifiacation and segmentation)
chemical digestion (in the large intestine)
hydrolysis of macromolecules (break down using water and enzymes)
lipid digestion  ??
protein digestion  aminoacids
carbohydrate digestion  glucose,fructose, galatose
nucleic acid digestion  sugar + phospahte + nitrogen base
Carbohydrate digestion
almost all in the small intestine (pancreatic amylase and brushborder enzymes) a little bit in the mouth (salivary amylase)
brush border enzyme starts at the amine free side and breaks amine groups off of aminoacids/protiens
does the same as aminopeptidase but only work on dipeptide chains
Peyer's Patch
Concentration of lymph tissue
Small intestine blood supply
superior meseteric artery, to superior mesenteric vien to hepatic portal vien
Small intestine nerve supply
splenic and vagus nerves
digests RNA broken down into nucleotides
digests DNA broken down into nucleotides
nucleosidease and phosphatase
breaks down nucleotides
The above give you pentose sugar, phosphate & nitrogenous bases
this is a brush border enzyme
fat digestion
start with trigylcerides
pancreatic lipase/bb lipase break it down into 3 fatty acids and gylcerol
emulsified by bile salts in the small intestine (this makes the micelles which are then broken down by the above)
Regular absorption
Monosaccharides,AA, dipeptides and tripeptides, glycerol
absorbed via active transport into the blood/capillaries
Absorption via lacteals
Fatty acids, monogylcerides, and cholesterol
lacteals --> thoracic duct --> subclavian vein
extrinsic salavary glands
are not embedded in tissue
paratiod gland
(infront of your ear secretes into top portion of the mouth) infection of this gland gives you the mumps
sublingual gland
secretes on the the floor of your mouth
submandibulare gland
secrete into the back of the mouth
buccal glands
secrete a tiny bit of mucous into your mouth) not a real issue
Composition of salivary glands
2 types of cells :
serous cells make enzymes
mucous cells make mucous
combine the two to get saliva
Composition of saliva
99 % water
HCO3 bicarbonate ion maintains 7.0 pH
salivary amalyase, IgA (antibody), electrolytes, metabolic waste
Controling nerves of the salivary glands
parasympathetic control via the facial nerve if sympathetic nerves are inervated then your mouth becomes dry
buccal phase of degultanation chewed (mastication) and mixed with saliva
2.tongue roles food into bolus and pushes back into pharynx
3.tongue presses against soft palate sealing the oral cavity
4.soft palate pushed up by bolus
phryngeal phase of degultanation
1.bolus triggers nerves (CN V AND IX) medulla
2.hyoid and larynx elevated so epiglottis covers top of larynx
3.Soft palate raises
Esophegeal phase of degultanation
1.muscles in pharynx relax to open an open the upper esophageal sphincter
2.peristaltic wave begins to force food down esophagus
3.when wave hits stomach lower esophageal sphincter relaxes and opens to let food in
chemical digestion of the stomach
acid (HCl) is produced at a pH of 2 which activates pepsin
pepsin (hydrolises protien) and renin (not responsible)
neural control of the stomach/digestion
parasympathetic(vagus nerve) increases contractions and secretions
sympathetic(splenic nerve) decreases contractions and secretions
Cephalic phase of digestion
All reflexes
Thought, taste, smell stimulates secretions
Stimulation from brain to stomach via vagus
To decrease this bc upset working out, etc you get a signal down the splenic nerve (or your vagual tone is decreased)
Stimulation is on the interic plexus  submucosal plexus
Gastric phase of digestion
Stretch receptors  stretch from food stimulates contraction and enzyme release more you eat the fast you will digest
Caffine, histamines increase secretions
Chemoreceptors: raise the pH so the body secretes more
This all causes the release of gastrin

pH lower then 2
intestinal phase of digestion
a.k.a. inhibitory phase
Chyme enters intestines with pH of 2
Stretch of the small intestines
both stim intestine to release hormones
Short reflexes (enterogastic reflex)
stretch here inhibits stomach  on the enteric system
Long reflex
inhibition from brain of vagual tone
Usually caused by extreme stretching of stomach or small intestine or presence of irritants in stomach (e.g., bacterial toxins, excessive alcohol, spicy foods, certain drugs)
emetic center initiates impulses to
contract abdominal muscles (increases intra-abdominal pressure)
relax cardiac sphincter
raise soft palate (closes off nasal passages)
excessive vomiting results in dehydration (electrolyte blance off) and alkalosis
Carbohydrate Absorption
>Absorption into epithelial cell
>glucose & galactose----helped by sodium symporter(active transport) from the intestinal juice
>fructose on its own facilitated diffusion
>Movement out of epithelial cell into bloodstream
by facilitated diffusion
Absorption of AminoAcids
>Absorption into epithelial cell active transport with Na+ or H+ ions (symporters)
>Movement out of epithelial cell into blood Facilitated diffusion
>Large protein molecule absorption accounts for passive immunity and food allergies
fat absorption
Fats diffuse straight into the cells
FA and monogylcerides united in the smooth ER to my trigylcerides
Golgi apparatus packages with protien ^ and cholesterol  Chylomicron
Dumped into the lacteal
electrolyte and vitamin absorption
Ca, Fe, and B12 are the only ones that are regulated and not absorbed by a diffusion based system
Hormone calcitriol made from Vitamin D used for Ca reg
Ferritin a protien in order to ferry the iron
Intrinsic factor is used to take in B12
Pancreatic islets
produce insulin and glucagon
Acinar cells
in the pancreas create enzymes upon stimulation of CCK
Travels of the pancreatic juice
Stuff into pancreatic juice > pancreatic duct >common bile duct >hepatopancreatic ampulla > opens into intestine onto the duodenal papilla
Pancreatic Juice
Pancreatic amylase,
Pancreatic lipase,
Pancreatic nuclease
HCO3 ions
Regulation Nervous and Hormonal
Vagus nerve parasympathetic nerve stims release of juices
CCK bc of fats efftects acinar cells
Secretin bc of pH effects HCO3
GIP bc FA and glucose insulin release
Liver function
CHO metabolism to help maintain blood glucose levels
Lipid metabolism: synthesize, lipids and cholesterol
Converting CHO and Protein to fat
Protein metabolism
Deamination of protein
Forming urea
Synthesizing clotting factors

Storage glycogen, iron, vitamin A, D, B12
Destroy damage red blood cell
Secretes bile
blood supply to the liver
Hepatic portal vein
nutrient rich blood from stomach, spleen & intestines
Hepatic artery from branch off the aorta
Both drop into capillary know as liver sinusoid
After sinusoid goes to central vein (still in the liver) then into hepatic vein
Then into inferior vein cava
30% of blood comes in the hepatic artery
Microscopic liver
Hepatocytes – actually doing the functions
Lobes are broken up into smaller portions called lobules
Lobules consist of 6 portal triads and one central vein
Bile formed in these cells then put in bile caniculi (run the oppostie direction to outside of the lobule)
Out side of the lobule is bile duct all bile caniculis dump here
Bile ducts
Bile ducts merge until you have a right and left hepatic duct
These merge to form the common hepatic duct leaving the liver  merges with the cystic duct from gallbladder (form the common bile duct)
Common bile duct merges with common pancreatic duct to form ampulla (opens into the intestines) controlled by sphincter bile backs up into the gallbladder (Storage)
Yellowish, brownish or olive-green liquid
Water, bile salts, bile pigment, cholesterol, electrolytes
pH 7.6-8.6
Produced by the liver
Stimulated by bile salts returning via hepatic portal blood
Stimulated by secretin (hormone secreted by small intestine in response to fats in chyme)
Bile salts stimulate liver to make more bile (positive feeback)
Bile’s high pH acts as a bicarbonate buffer from the stomachs low pH
contents of bile/bile salts
Cholesterol derivatives
Enhance absorption of fatty acids, cholesterol, Vitamin A,D,E,K

Recycled via enterohepatic circulation
If insufficient bile salts or excessive cholesterol results in gallstones
contents of bile/bile pigments
Waste product of RBC
Conjugated bilirubin
Some absorbed by blood
Some stay intestine
Urobilinogen (stercobilin)
decreases blood sugar
supports glycolysis, and glucogenisis
decreases lypolysis
human growth hormone
supports Glycogenolysis and glyconeogenisis
increase lypolysis
supports raising blood sugar levels
Glycogenolysis and glyconeogenisis
increases lypolysis
increases lypolysis
supports Glycogenolysis and glyconeogenisis to help raise blood sugar levels in your blood
suports Glycogenolysis and glyconeogenisis
increases lypolysis
raises blood sugar levels
Anaerobic Respiration
if no mitochandrian or O2 present then pyruvic acid will be turned into lactic acid
Kreb's Cycle Plus Electron Transport chain
C6H1206 + 6 02  6 CO2 + 6H20 + 36 ATP
supports lypolysis
means gluconeogenisis, break down of glucagon (Glycogenolysis)
composed mostly of exogenous trigylcerides made in the small intestine wall
shipped to the lacteals goes out to fat cells liver cells (low density very little protien)
mostly trigylceride formed in the liver go from the liver to adiposecytes
mostly cholesterol made in the liver liver to any body cells
too many gives you authorosclerosis
these products are used to make cell wall and hormones
if no cholesterol is needed then it creates plaques (build up in the smooth muscle tissue)
cholesterol from cells back to the liver very high density better for you cause your liver can get ride of the fat/cholesterol
Ratio of Cholesterols
TC < 200mg
LDL <130 mg
HDL > 40 mg
Tryglycerides 10-190

TC/HDL = risk factor 4+ is bad
Liver role in metabolism
Fat metabolism
Packages fatty acids into forms that can be stored or transported
Stores fat
Forms lipoproteins for transport of fats, fatty acids and cholesterol to and from other tissues
Synthesizes cholesterol (from which it can synthesize bile salts)
The Postabsorptive state (maintain glucose levels)
From the end of the absorptive state to the next meal
Body relies on reserves for energy
Liver cells break down glycogen, releasing glucose into blood
Liver cells synthesize glucose (gluconeogenesis)
Lipolysis increases and fatty acids released into blood stream
Fatty acids undergo beta oxidation and enter Kreb’s cycle
Amino acids either converted to pyruvate or acetyl-CoA
Skeletal muscles metabolize ketone bodies and fatty acids
Skeletal muscle glycogen reserves broken down to lactic acid
Neural tissue continues to be supplied with glucose
Use anything to replace glucose oxidation
THe absorptive state
The period following a meal
Nutrients enter the blood as intestinal absorption proceeds
Liver closely regulates glucose content of blood
Adipocytes remove fatty acids and glycerol from bloodstream and storing TG
Glucose molecule are oxidized for ATP
Amino acids are used to build proteins