Physio Flashcards
major functions of GI tract
motility, secretion, digestion, absorption, excretion
upper esophageal sphincter
maintains highest resting pressure of all sphincters, and forward passage of material
lower esophageal sphincter
separates esophagus and stomach. consists of smooth muscle that relaxes during swallowing. coordinates passage of food into stomach and prevents reflux
pyloric sphincter
separates the stomach from duodenum. resting pressure contributes to regulation of gastric emptying and prevention of duodenal gastric reflux
ileocecal sphincter
separates ileum and cecum, prevents backflow of colonic contents into the ileum
internal and external anal sphincters
internal (smooth muscle) and external (skeletal muscle) control elimination of waste products
enteric nervous system
branch of the ANS with plexuses (myenteric and submucosal)
myenteric plexus
between the longitudinal and circular muscle layers of the GI tract, goes from end of esophagus to rectum. stim increases tonic contraction of the gut, intensity of rhythmic contractions, and velocity of conduction of excitatory waves which enhances peristalsis
submucosal plexus
between the circular muscle and submucosa in the small and large intestines. controls local intestinal secretions, absorption, and contraction of the muscle
types of receptors in the ENS
mechano, chemo, osmo, along with parasympathetic fibers
segmental/mixing contractions
chyme distends the walls which causes local contractions mixing chyme with secretions. 2/3 per minute
peristaltic contractions (myenteric reflex)
move material form mouth to colon, relatively weak contractions. 3-5 hours needed to go from pylorus to ileocecal valve
gastroileal reflex
triggers opening of the ileocecal valve to allow chyme through
enterogastric reflex
decreases gastric motility and secretions and contracts pyloric sphincter
pathological ileus
state where normal periods of quiescence are much longer. inhibitory neurons are abnormally active
migrating motor complex
contractions that pass down the stomach and small intestine
motilin
made in duodenal mo cells, released into circulation and stimulates contractions during active phase
deglutition
swallowing. voluntary and involuntary events.
pharyngeal phase
areas near the pharyngeal opening transmit impulses through CN v and IX which initiates swallowing
GERD
gastroesophageal reflux disease. failure of the ability to maintain the lower esophageal sphincter
achalasia
when lower esophageal sphincter fails to relax during swallowing
sections of the stomach
proximal gastric reservoir, distal antral pump
paracrines
released by endocrine cells of GI tract. act locally in same tissue that secretes them
neurocrines
made in neurons in GI tract and released following an action potential. diffuse across cleft and act on target cell
saliva functions
secreted by acinar cells, lubricates, protects, and has amylase in it
sjogren syndrome
autoimmune disease that distroys salivary and lacrimal glands.
xerostomia
dry mouth
kallikrein
activation of salivary glands releases this, resulting in production of bradykinin a vasodilator
oxyntic glands
inside surfaces of the body and fundus of the stomach. secrete mucus (mucous neck cells), pepsinogen/lipase (peptic cells), and HCl/intrinsic factor (parietal cells)
achlorhydria
lack of stomach acid secretion due to destruction of parietal cells
pyloric glands
secrete mucus for protection of pyloric mucosa from stomach acid. also secrete gastrin and somatostatin
pepsinogen to pepsin activation
at ph from 3-5, pepsinogen activates spontaneously to pepsin
alkaline mucous layer
protects gastric mucosa. erosive gastritis can result from NSAID use because it inhibits prostaglandin synthesis in stomach
stimulators of acid secretion
histamine, vagus, gastrin, insulin, caffeine, stress
inhibitors of acid secretion
somatostatin, glucose insulinotropic peptide, gastric inhibitory peptide, secretin
H2 receptor antagonists
effective as antacid agents because they block binding of ACh, gastrin, and histamine
cephalic phase
smelling, tasting, and conditioned reflexes stimulate HCl secretion through direct stim of vagus
gastric phase
Secretes HCl due to distension of stomach and presence of breakdown products of protein
intestinal phase
mediated by products of protein degradation, secretes HCl
pancreas
exocrine secretions into ducts then to the lumen (aqueous juice high in HCO3 from duct/centro-acinar cells and enzyme juice from acinar cells)
endocrine secretions into blood from islet of langerhans regulate blood sugar
pancreatic aqueous secretions
bicarb neutralizes stomach acid and allows enzymes to work at optimal neutral pH. pepsin inactivated at neutral. prevents dmg to duodenal and intestinal mucosa. dilutes enzyme juice (prevents it from becoming sticky)
pancreatitis
enzymes are released into the cell instead of being packaged into granules
secretion of chloride by acinar cells
NaCl secretion leads to influx of water and sodium into cell. ACh and CCK stim NaCl secretion
cystic fibrosis
defective CFTR channel, causing thick and viscous pancreatic secretions. messes with digestion. Pulmonary mucous is thick causing dyspnea and death
phases of pancreatic secretion
cephalic: more acini activation than ductal aqueous secretion.
gastric: distenstion of stomach induces vaso vagal reflex, gastrin stims acinar cells to make enzymes and parietal cells to make HCl
intestinal phase: secretin and CCK are made
secretin
released into blood from duodenal mucosa in response to acid in duodenum. causes duct cells to make aqueous secretion. “nature’s antacid” lots of bicarb
Cholecystokinin (CCK)
hormone released in response to protein digestion products or fatty acids. stims enzyme secretion by acinar cells. low volume, high enzyme content. causes gall bladder contraction to release bile. slows gastric emptying
rate limiting step in bile acid formation
addition of hydroxyl group by cholesterol 7 alpha hydroxylase. inactivated by bile acid, activated by cholesterol
choleretic
agent that stims the liver to increase output of bile
bile salts
amphipathic. can emulsify and solubilize fats and steroids. water soluble. conjugated with glycine or taurine in liver. bacteria deconjugate bile salts back to bile acids
formation of gallstones
supersaturation of cholesterol, nucleation and precipitation, then growth of microstones to form macrostones
cholecystitis
inflammation of gall bladder usually caused by blockage of the cystic duct by a gallstone.
insulin
made by beta cells which are located at the center of the islets of langerhans in the pancreas. it is an anabolic hormone secreted in times of excess nutrient availability. calls for storage of energy
glucagon
catabolic hormone, secreted during food deprivation. allows utilization of stored nutrient reserves by mobilizing glycogen, fat, and protein
somatostatin
paracrine hormone that inhibits release of insulin and glucagon as well as gastrin, gastric acid secretion, and all gut hormones
islet of langerhans
in pancreas. beta cells in center secrete insulin, proinsulin, and c-peptide. alpha cells at periphery secrete glucagon. delta cells in periphery secrete somatostatin. blood flow is from center to periphery.
pancreatic polypeptide
made by F cells in periphery of islet of langerhans. inhibits gall bladder contraction and inhibits pancreatic exocrine secretion during strenuous exercise, after ingestion of a protein rich meal, or during hypoglycemia
glucagon synth and degradation
made as 160 AA pre-proglucagon. processing yields glucagon, glicentin, glicentin like peptide, glucagon like peptides 1 and 2. glucagon is degraded in liver and kidney, very little excreted.
stimulators of glucagon secretion
hypoglycemia, increase in arginine and alanine (indicative of protein degradation), exercise, stress
inhibitors of glucagon secretion
somatostatin, insulin, hyperglycemia
effect of glucagon on liver
antagonizes action of insulin by stimulating glucose output via gluconeogenesis and glycogenolysis and increased lipolysis. activates protein kinase A, which phosphorylates enzymes.
insulin synth and degradation
synthed in preproinsulin form. packaged in golgi and processed. secreted in granules with zinc which form 6 insulin molecules into hexamers. cleaved to insulin and c-peptide. c-peptide gets secreted in urine and is used to detect insulin levels
insulin secretion by beta cells
glucose picked up by b cells, used to make ATP. elevated ATP inhibits potassium channel and depolarizes cell. voltage gated Ca channels open, and Ca comes in. this causes release of insulin granules. AA levels increased also lead to elevated ATP.
glucagon stimulation of insulin secretion
glucagon binds G alpha B receptor and activates protein kinase A, which raises Ca concentration and inreases exocytosis. somatostatin binds G alpha I and inhibits protein kinase A
incretins
CCK and GIP, glucagon-like peptide 1
provide advance notice of feeding and stimulate insulin secretion: oral glucose yields more insulin than IV glucose
catecholamines and insulin during exercise
insulin secretion up due to epinephrine. local innervation through norepinephrine acts through alpha receptor and predominates. net result is to suppress insulin secretion and prevent excess glucose uptake. allows liver to supply glucose and fatty acids to muscle
action of insulin on liver
stimulates glucose uptake and decreases glucose output. stims formation of glycogen and inhibits glycogenolysis. promotes glycolysis and lipogenesis.
action of insulin on muscle
stims glucose uptake by increasing GLUT-4 and promotes glycogenesis while inhibiting glycogenolysis. supplies acetyl CoA for fatty acid synth
action of insulin on adipocyte
stims glucose uptake via GLUT-4 and increases glycolysis, leading to upped alpha glycerophosphate which leads to increased esterification of fats. decreases lipolysis. makes fattty acids but inhibits them to be used as an energy source
glucose tolerance test
can diagnose diabetes. diabetes if plasma glucose is higher than 200 mg/dL at the second hour
type 1 diabetes
insulin deficiency
insulinemia
high insulin in blood
glucagon deficiency
rare
glucagonoma
high levels of glucagon in blood, causes hyperglycemia
orixigenic factors
neurotransmitters that stim feeding (neuropeptide Y)
anorexigenic factors
inhibit feeding. corticotropin releasing hormone, GLP-1, alpha MSH, CART
CCK
(I cells) diffuses locally in a paracrine fashion. sends message that ingested fat/protein is being processed and will soon be absorbed
ghrelin
secreted from oxyntic glands of stomach. stimulates food intake.
leptin
derived from white adipocytes. influences energy homeostasis. stimulate receptors to reduce food intake, inhibit AgRP and NPY (which stim food intake)
leptin and leptin receptor mutations cause obesity
MC4R receptor mutation
cause obesity. receptor for alpha melanocyte stimulating factor from POMC neurons
folds of kerckring
finger like projections that stick into the lumen
celiac disease
decrease in absorptive surface area due to a reduction in the number and size of microvilli
enterocytes
absorptive cells that make up villi. they are columnar epithelial cells in a single layer
goblet cells
secrete mucous in response to Ach released from parasymp cholinergic nerve fibers.
crypt
undifferentiated cells of the crypt secrete NaCl into lumen and water follows osmotically. crypt cells move up the villi and eventually become absorptive cells
transcellular pathway
transfer of materials across the brush border, through the cytoplasm, and then across the basolateral membrane
shunt pathway
aka paracellular pathway. through tight junctions and the extracellular space
brush border
aka apical membrane. has glycoprotein matrix and is major membrane for absorption of nutrients. contains etoenzymes that complete digestive process
basement membrane
aka lamina propria, contains capillaries and lacteals
water absorption
drudoenum and upper jejunum, completely absorbed by end of jejunum
what does ileum absorb?
fluid and electrolytes, along with B12 and ionized bile salts. if jejunum is removed, ileum can adapt and take over its role
what does duodenum absorb?
calcium and iron
what does jejunum absorb?
jejunal enterocytes absorb Na+ and HCO3-, along with glucose and amino acids.
how does Na+ enter jejunal enterocyte?
Na/glucose and Na/amino acid cotransport.
Na/H antiport, keeps internal pH of enterocyte near neutral
NaCl absorption by ileal absorptive cell
enter via Na/H antiport in parallel with Cl/HCO3 exchange. Cyclic AMP inhibits NaCl absorption by ileum.
vipoma tumors
secrete a lot of VIP, resulting in greatly decreased NaCl absorption leading to increased osmolarity in lumen and diarrhea
cholera
toxin increases cAMP, inhibits NaCl absorption, increases NaCl secretion by jejunal crypt cells.
absorption of iron
heme iron. iron is absorbed as heme, then the iron is freed within the cell.
non-heme iron. Fe++ forms insoluble complexes with food, but is released by gastric acid. Some Fe++ goes to Fe+++ and is secreted. Fe++ absorbed via cotransport with a proton
calcium absorption in duodenum
passive paracellular absorption occurs throughout small intestine. Active transcellular absorption occurs only in duodenum. Ca enters thru channel, and is taken in by organelles. the enterocyte extrudes Ca across basolateral membrane thru Ca pump and Na/Ca exchanger. Vitamin D stimulates all three steps of absorption.
long term regulation of calcium
increased absorption of Ca inreases plasma concentration of Ca, which decreases parathyroid hormone secretion which inhibits formation of active vitamin D, which decreases synth of calbindin, which decreases absorption of Ca
enterokinase
trigger for intestinal protein digestion. converts trypsinogen to trypsin. trypsin then activates endo and exopeptidases yielding chymotrypsin, elastase, and carboxypeptidase A and B
exopeptidases
carboxypeptidase A and B
endopeptidases
trypsin and chymotrypsin
absorption of amino acids
most AAs are mediated by Na coupled AA transporters. transport against concentration gradient. Na out, AA in.
absorption of oligopeptides
done by PepT1, an H+/oligopeptide cotransporter. moves oligos across apical membrane
hartnup disease
system B apical membrane AA transporter. this reduces absorption of neutral AAs. a lot of tryptophan is excreted in the urine
cystinuria
system B 0 AA transporter is defective. absorption of cystine and basic AA is reduced. cystine makes kidney stones
ptyalin
salivary amylase, begins conversion of starch to sugars. inactivated in the stomach, works best at pH 6.7
digestion and absorption of sugars
glucose and galactose compete for the same Na-coupled carrier.
glucose-galactose malabsorption
rare genetic disease in which Glc/Gal carriers (SGLT1) are missing/bad. accumulation of Glc in intestine causes diarrhea, dehydration, and death. restricted to fructose diet since that can be absorbed
cholecystokinin
CCK. released in duodenum due to presence of fats. slows gastric motility, stimulates pancrease to make enzymes, stims intestinal fluid secretion and gall bladder contration, relaxes sphincter of oddi
micelles
include long chain fatty acids, cholesterol, monoglycerides, phospholipids, bile salts, fat soluble vitamins
NPC1L1
niemann-pick C1 like 1. used to absorb cholesterol.
ApoB48
key component of chylomicrons. chylomicrons also depend on microsomal triglyceride transfer protein, MTP. Transports newly formed apoproteins to the chylomicrons
abetalipoproteinemia
visible fat laden enteroctes duee to MTP mutation. decreased plasma triglyceride and cholesterol levels, and deficiencies in fat soluble vitamins
micturition
the process by which the urinary bladder empties when full
detrusor
smooth muscle of the bladder. contraction helps with emptying the bladder
pontine micturition center
controls the detrusor muscle and the urinary sphincters
suprapontine center
exert tonic inhibition over the pontine micturition center providing voluntary control
autonomous neurogenic bladder
sacral spinal centers damaged. lower motor neuron
benign prostatic hyperplasia/hypertrophy
enlargement of prostate gland, squeezes the urethra. lead to more frequent urination, dribbling/leakage, weak stream, urgency
constipation
results from poor motility which leads to greater absorption of liquids and hard feces
diarrhea
rapid movement of fecal matter through the large intestine causing little absorption
osmotic diarrhea
results from non-absorbable solutes in the lumen (lactase deficiency/lactose not broken down)
secretory diarrhea
results from excessive secretion of fluids by crypt cells due to bacterial overgrowth
ileocecal valve
separates the small and large intestine. prevents backflow of fecal matter from colon to small intestine
gastroilieal reflex
activated when food enters the empty stomach. intensifies peristalsis of the small intestine and relaxes the ileocecal sphincter allowing passage from ileum to colon
what does colon absorb?
absorbs Na, Cl, and H20 and secretes K and HCO3
mode of active Na absorption by large intestine
Na-H and Cl-HCO3 exchange is coupled by a change in intracellular pH that results in electroneutral NaCl absorption. creates an osmotic gradient across intestinal mucosa, promoting absorption of water. Na channels are also used in the entire colon allowing H20 and Cl to follow passively through intracellular tight junctions
haustrations
specialized for slow segmental propulsion and mixing, allowing time for electrolyte and fluid absorption, solidifying the chyme
taenia coli
3 flat bands of longitudinal muscle
gastrocolic reflex
increased incidence of mass movements, which force the chyme/feces towards the rectum
hirschsprung’s disease
present at birth. lack of ENS in the distal part of the GI tract. obstructive syndrome in infants or constipation
defecation reflex
triggered by distension of rectum. sensed by mechanoreceptors which activate myenteric nerves. fortified by parasymp defecation reflex
