GIT PHYS Flashcards
wen u have taste smell, thought of food etc, the stimulation to get salviation is via
parasymp nerves
ptyalism/drooling
treated by atropine (muscarinic antagonist) -start with low dose
serostomia (dry mouth) diagnosis n treatment
5% citric acid
swallowing difficulty (ask pt to swallow dry biscuit without water)
treat cause first then use muscarinic antagonist
para activation on salivation
get lots of more saliva output
response is sustained (over long time)
if u chop of para nerve- u get decreased secretion AND atrophy of salivary glands
sympa activation on salivation
get only a little bit more of saliva output
response is only for short time (transient)
if u chop of sympa nerve (denervate it)- get decreased secretion only
mucus cells release
mucus
parietal cells release
intrinsic factor and hcl
chief cell release
pepsinogen
enteroendocrine cells:
ECL and G
ECL-histamine
G-gastrin
wat cells are where in gastric gland?
mucus on top
then parietal n chief
then enteroendocrine
pernicious anemia
we need it B12 for maturation of rbc.
no parietal cell=
no inrinsic factor
=no vit b 12 absorption
pepsin works at what ph
around 1.8 to 3.5 it
if ph above 5, it doesn’t work
STIMULATION OF PARIETAL CELLS ie RECEPTOR MEDIATED ACID SECRETION
Gastrin, histamine, Ach can act on receptors to stimulate parietal cells to release more HCL
STIMULATION OF PARIETAL CELLS ie RECEPTOR MEDIATED ACID SECRETION
- via ACH, HISTAMINE and GASTRIN acting directly onto the receptors
- via gastrin doing long way
- Via Ach doing long way
- Caffeine
Somatostatin
inhibits HCL secretion
things that stimulate HCL secretion from parietal cells?
Gastrin, histamine, Ach
caffeine –get more acid secretion when theres too much caffeine
long way of gastrin stimulating HCL secretion from parietal cell
- meat or protein food stimulate G cells to release gastrin
- when gastrin is released, it stimulates ECL cells to relase histamine
- histamine tells parietal cells to release HCL and intrinsic factor
STIMULATION OF PEPSINOGEN RELEASE
- by each from vagus nerves/gastro enteric nervous plexus
2. acidity in stomach (not much. mainly no. 1^)
cephalic phase of HCL secretion
stimulus: semll, sight sound, chewing, thought of food, taste
stimulates parietal cell to release HCL via Ach n gastrin
gastric phase of HCL secretion
stimulus: distention of stomach, presence of semi digested proteins, an increase in ph (more alkaline)
stimulates parietal cell to release HCL via Ach n gastrin
intestinal phase of HCL secretion
stimulus: stretch of duodenum, protein digested products
inhibits secretionof hl by decreasing Ach and gastrin secretion
exocrine
into duct
endocrine
into blood stream
pancreas exocrine ducts
secretes pancreatic juice
pancreatic juic
• =pancreatic enzymes + sodium bicarbonate
is alkaline
pancreatic enzymes that are inactive wen secreted
- trypsinogen
- chymotrypsinogen
- carboxypolypeptidase
pathway fro secretion of proteolytic enzymes from pancreas
- trypsinogen activated to trypsin by enterokinase
- trypsin then activates a lot of stuff
a. chymotrypsinogen into chymotrypsin
b. procarboxypolypeptidase into carboxypolypeptidase
c. trypsinogen into trypsin
sodium bicroabonate (component of pancreatic juice) is released by
epithelial cells of the ductules and ducts.
enzymes (component of panreatic juice) released by
acini cells
at top of intestine, ACIDITY of chyme stimulates release of
secretin from S cells
at top of intestine, ACIDITY of chyme stimulates release of
secretin from S cells
at top of intestine, FATTINESS of chyme stimulates release of
CCK from T cells
secretin job
at pancreas: stimulates the release of a sodium bicarbonate water solution at pancreas
at liver- stimulates the ductal cells to secrete an alkaline or bicarbonate solutions
cck job
o CCk stimulates release of pancreatic enzymes at pancreas
also comes down onto gall bladder (tells gall bladder to constract) AND relaxation of Sphintor of Oddi
secretin job
stimulates the release of a sodium bicarbonate water solution at pancreas
cck job
o CCk stimulates release of pancreatic enzymes at pancreas
also acts on gall bladder (tells gall bladder to constrict)
Ach going to pancreas does what
stimulates the pancreas to release pancreatic enzymes
in cephalic n gastric stage
longitudinal smooth muscles cells does wat
• SHORTENING OF THE GUT (ie vertically) will involve longitudinal cells
circular cells
• CONSTRICTION OF THE GUT (ie horizontally will involve circular cells
oesophageal peristalsis
above the bolus, have constriction
below the bolus, have shortening
sympa actiavtion on sphinctor=
closes sphinctor
parasympa n myenteric plexus on sphinctor
relaxes/opens sphinctor
autonomic nerves are in
circular smooth muscle layer
para symp on gut motility n secretion
aCH will increase gut motitly n secretion
MOTILITY OF THE SMALL INTESTINE
o Segmenting contractions
o Migrating Myoelectric Contractions
MIGRATING MYOELECTRIC COMPLEX:
wen ur not eating/no food in entering stomach
stomach to the large intestine
initiated by increase in
chypme PH or motlin
(eating stops release of motilin)
MOTILITY OF LARGE INTESTINE
Haustral contractions
Mass movements
Wen u defaecate:
o Rectum contracts
o Internal anal sphincter relaxes
o External anal sphincter relaxes
HIRSHPSRUNG DISEASE
FROM Aganglionic megacolon
achalasia
lower oesophageal sphinctor fails to relax
portal triad
hepatic artery
hepatic portal vein
bile duct
pathway of bile seccretion
liver cannaliculi terminal Bile duct hepatic duct common bile duct (duo or cystic duct into gall bladder
leptin
makes u feel full hormone
acts on arcuate ..of hypothalamus
tells brain about fat: more fat=more leptin=less hunger
decreases NPY expression
in obesed ppl-decreased sensitivity to leptin
low leptin=low reproductive hormone levels
increased leptin= increased thermogenesis
ghrelin
makes u feel hungry hormone
secreted wen stomach is empty
leptin
makes u feel full hormone
acts on arcuate ..of hypothalamus
tells brain about fat: more fat=more leptin=less hunger
decreases NPY expression
in obesed ppl-decreased sensitivity to leptin
low leptin=low reproductive hormone levels
increased leptin= increased thermogenesis
spring= leptin effective
autumn=leptin not effective
