Physiology Flashcards
source of gastrin
G cells in antrum of stomach and duodenum
source of somatostatin
D cells in pancreatic islets and gi mucosa
source of CCK
I cells in duodenum and jejunum
source of secretin
S cells in duodenum
source of GIP
K cells in duodenum and jejunum
source of motilin
small intestine
source of VIP
para ganglia in sphincters, gall bladder and small intestine
what cells found in duodenum and secreted what
G cells - gastrin I cells - CCK K cells - GIP S cell - secretion D cells - somatostatin
what cells found in jejunum and secrete what
I cells - CCK
K cells - GIP
function of gastrin
increased H secretion
growth of gastric mucosa
increased gastric motility
stimulation of gastrin
stomach distension
alkalinisation
amino acids/peptides
vagus
inhibition of gastrin
decreased pH < 1.5
what causes gastrin to increased pathologically
h pylori chronic atrophic gastritis
Zollinger Ellison syndrome
chronic PPI use
what are actions of somatostatin
decreased H secretion decreased pepsinogen secretion decreased pancreatic fluid secretion decreased intestinal fluid secretion decreased gall bladder contraction decreased insulin release decreased glucagon release
what stimulats somatostatin
increased by acid
what decreases somatostatin
decreased by vagus
what is octreotide
somatostatin analogue
treatment for acromegaly
octreodtide
treatment for insulinoma
octreotide
treatment for carcinoid syndrome
octreotide
treatment for variceal bleeding
octreotide
what does CCK do
increase pancreatic secrtion
increases gall baldder contraction
decreases gastric emptying
increases spincter of oddi relazation
what stimulates CCK
fatty acids
amino acids
how does CCk cause pancreatic secretion
acts on neural M pathways to increased pancreatic secretions
what does secretin do?
increases pancreatic HCO3 secretion
decreases gastric acid secretion
increases bile secretion
what stimulates secretin
acid
fatty acids in lumen
NO PROTEIN
why is the action of secretin important
neutralized acid from the stomach to permit action of pancreatic enzymes
what does GIP stand for?
flucose-dependent insulinotropic peptide
what does GIP do?
decrease H secretion
increases insulin release - if oral, not IV
what stimulates GIP?
fatty acids
amino acids
oral glucose
what does motilin do?
produces migrating motor complexes
MMC
what stimulates motilin
increases in fast
what is a motilin receptor angonist
erythromycin
what is a drug that can be used to stimulate intestinal peristalsis and why?
erythromycin bc tis a motilin receptor agonist
what does VIP do?
increases intestinal water and electrolyte secetion
increase relaxation of intestinal smooth muscle and sphincters
~~think of clinical implications for VIPoma~~
what stimulates VIP?
distension
vagal
what inhibits VIP
adrenergic
copious watery diarrhea
hypokalemia
achlorhydria
VIPoma, non alpha, non beta islet cell tumor (VIP increases intestinal water and electrolyte secretion and realizes intestiona smooth muschle and spinhters.
what does NO do?
increased smooth muscle relaxation includint the LES
what pathology does the significance of NO relaxation of the LES exist in?
achalasia
bird beak
what hormones cause H secretion
gastrin
ach
histamine
what hormones cause decreased H secretion
somatostatin
secretin
GIP
what hormones increased pancreatic secretion
CCk
secretin
GIP (insulin)
what hormones decrease pancreatic secretion
somatostatin
what hormones have an effect on smooth muscle?
gastrin - increases gastric motility
somatostatin - decreased gall bladder contraction
CCK - gall bladder contraction, decreased gastric emptying, increased sphincter of oddi relaxation, VIP - increased intestinal and water electrolye secretion and relaxation of intestinal smooth muscle and sphincters
NO: relaxation of spnihcters including LES
what hormones are stimulated by aa/protein?
gastrin
CCK
NOT SECRETIN
GIP
what hormones are stimulated by fatty acids
CCK
secretin
GIP
what hormeones are stimulated by oral glucose and not IV glucose
GIP
what hormones are stimulated by distension
VIP
gastrin
what hormones are stimulated by vagus
gastrin
VIP
where are parietal cells located
body/fundus of stmach
what do parietal cells make?
HCL and intrinsic factor
what causes parietal cell destruction
chronic gastriris
pernicious anemia
what stimulates gastric acid production
stimulated by histamine, ach and gasrin
what inhibits gastric acid prodcution
somatostatin
GIP
PG
secretin
what is a gastrinoma
gastrin secreting tumor that causes high levels of acid and ulcers refractor to medical therapy (like PPI)
where does pepsinogen come from
chief cells in the body
where does pepsin come from
pepsinogen in an acid environment
what stimulates pepsinogen relase
vafal stimulation
local acid
where does HCO3 come from
mucosal cells @ fundus of stomach, duodenum, salivary galnds, pancreas and brunner glands in the duodeunm
what stimulats HCO3 secretion?
increased when pancreatic and biliary secretinos increased
secretin
how does gastrin exert effects on parietal cells
mostly indirectly through stimulation of ECL to produce histamine
also directly on pariental cells
ENDOCRINE
list the receptors on parietal cells
M3 receptor CCKb H2 receptor SST receptor PG receptor
list the receptors that are Gi
PG receptor
SST receptor
list the receptors that are Gs
h2 receptor
list the receptors that are Gq
CCKb
M3 receptor
what cause the alkaline tide
water and carbon dioxide form bicarb and hydrogen inside parietal cells. h is extruded from cell via HKATPase and HCOe goes to blood in exchange for CL that also leaves into the lumen to combine with H to fomr HCl.
what else can act on the pg receptor
misoprostal - inhibits
where do proton pump inhibitors work
on the HKATPase that’s shooting H out to stomach and K into cell.
describe pancreatic secretions
isotonic always
pancreatic secretions low flow
high Cl, normal Na (high), normal K (low)
pancreatic secretions high flow
high HCO3, normal Na (high), normal K (low)
what is role of alpha amylase
starch digestion
how is alpha amylase secreted
in active form
what are lipases for
fat digestion
what are proteases for
protein digestion
list the proteases
trypsin, chymotrypsin, elastase, carboxypeptidases
how are proteases secreted
as zymogens that are activated in the duodenum by trypsin
describe how tryspinosgen is crucial to protein digestion
gets activated by enterokinase/enteropeptidase a brush border enzyme of the duodenum and jejunum so it can become active trypsin to activate other zymogens/proteases
where do you find enterokinase/enteropeptidase
brush border of duodenum and jejunum
how are carbs absorbed?
as monosaccharides: glucose, galactose, fructose
describe how monosaccs are absorbed at apical membrane
SGLT-1: Na dependent for glucose and galactonse
GLUT5: fructose, facilitated diffusion - cannot be absorbed vrs a concentration gradient
how are monosaccs absorbed at basolateral membrane?
GLUT2 facilitated diffusion
how do you distinguish GI mucosal damage from other causes of malabsorption
D-Xylose absorption test
where is Fe absorbed
as Fe++ in the duodenum
where is folate absorbed
in the small bowel
where is B12 absorbed
terminal ileum with bile salts
needs IF
describe histo and location of a peyers patch
unencapsulated lymphoid tissue in the lamina propria and submucosa of the ileum
what is an M cell?
specialized epi cells that sample and present antigens to immune cells
What happens when a moo is encountered in an M cell?
B cells are stimulated in germinal cenetres to differentiate into IgA secreting plasma celsl which ultimately reside in the lamina propria. Ig A gets protective secretory component and is transported across the epithelium to the gut to deal with the intraluminal antigen
what makes up bile
bile salts (primary conjugated with glycein or turaine - water soluble), phospholipids, cholesterol, bilirubin, water, ions
what is the rate limiting step in bile synthesis
cholesterol 7alpha hydroxylase
who cares about bile
everyone
why do we care about bile
digestion and absorption of lipids and fat soluble vits ADEK
cholesterol excretion
anti moo via membrane disruption
what is bodys only way to get rid of cholesterol
bile (what about people without a gallbladder!! give them bile acids and watch their cholesterol and atherosclerosis!?)
how does bile protect vrs moos?
membrane disruptionq
list the steps in bilirubin form heme to poop and pee :)
@ RES: heme - hemeoxygenase - biliveridin - reductase - bilirubin
@ blood: unconjugated bilirubin - albumin
@ liver: OATP passive transport of unconjugated bilirubin – UDP glucoronosyl-transferase - conjugated bilirubin – MRP2 active transport
@ gut bacteria: conjugate bilirubin – urobilinogen
@ feces: stercobilin brown
@ circulation : urobilinogen 90% of 20% back to lvier and 10% of 20% to urobilin and urine
which bilirubin is water soluble
direct/conjucated
CONSENANTS
which bilirubin is water insoluble
insoluble - vowels
indirect/uncongucated
vitamin D deficicency
rickets: bone pain and deformity
osteomalacia: bone pain and muscle weakness
hypocalcemia tetany
supplement breast milk
vitamin E deficiency
hemolytic anemia, acanthocytosis
muscle weakness
posterior colomn and spinocerebellar tract demyelination
vitamin A deficiency
night blindness - nyctalopia dry, scaly skin - xerosis cutis corneal degeneration - keratomalacia bitot spots on conjunctiva immunosuppression
vitamin K deficiency
neonatal hemorrhage with increased PT and aPTT and normal bleeding time
give injection at birth - not in breast milk
what vitamin deficiencies can cause anemia
vitamin E - hemolytic
B12 - megaloblastic macrocytic anemia
B9 - megaloblastic macrocytic anemia
B6 - sideroblastic anemia due to impaired hemoglobin synthesis and iron excess.
