GIT physiology Flashcards
Describe the anatomy of the stomach
major GI structure lying between oesophagus and dudenum and responsible for breaking down food to produce chyme.
has 4 main parts = cardia, fundus, body, antrum
lesser and greater curve.
fundus has distensible walls for food reservoir
antrum has thick walls for grinding and churning
ends in the pylorus - thick muscular funnel
inner surface has ruggae - irregular folds.
what level does the stomach sit?
T11 to L1
describe the layers of stomach - histology
mucosa = collumnar epithelium + lamina propriae + muscularis mucosa
submucosa
3 muscle layers -oblique, circular, longitundal
serosa - outermost layer
between the layers lies the myenteric plexus and the submucosal plexus
describe the structure of a gastric pit / gland
within the mucosa, the columnar epithelium invaginates into gastric pits which are openings of the gastric gland.
various cells line these and have a function in production of gastric acid and other substances for digestion.
name the main cells of the stomach and describe their action
Parietal cells = HCl + intrinsic factor. found in neck of gastric glands predominantley in fundus and body
neck cells = mucus and HCO3. found at the opening of the pits. protection
cheif cells = pepsinogen. found at the base of gastric glands. pepsinogen is precusor for pepsin which breaks down proteins (hydrolysis of peptide bond)
G cells = gastrin - found at base of the gland - stimulates acid production and gastric motility
Enterochromaffin cells = histamine - promotes acid release.
D cells = somatostatin - inhibits acid and gastrin release - in base of gastic gland.
what are the functions of gastric acid?
breakdown of proteins - denature and aid pepsins
activates pepsinogen to pepsin
kills microbes
improves absorption of Fe
what is the function of intrinsic factor?
intrinsic factor is a glycoprotein produced by parietal cells in the stomach
binds vitamin B12 = protecting it from breakdown and aiding absorption by terminal ileum
describe the innervation of the stomach…
intrinsic = myenteric plexus and submucosal plexus - pacemaker cells giving basal level of motility and sphincter control.
extrinsic = ANS
* sympathetic (coeliac plexus) (NA)- inhibits motility
* parasympathetic (ACh)- promotes motility and stimulates gastrin and histamine release hence HCL.
* inputs to ANS includ stomach distention
explain the biochemistry of HCL production..
- H20 + CO2 by carbonic anhydrase
- H/K ATPase luminal membrane
- HCO3 into blood with antiporter - chloride
- chloride channel on luminal membrane
secretion by parietal cells luminal surface
extensitve mitrochonidria, folds to increase S.A on membrane
describe the control of HCL release by parietal cells
on basolateral membrane is receptors - gastrin, histamine, M2
binding of these stimulates H/K ATPase
these 3 hormones directly stimulate acid production. others can indirectly by in turn stimulating/inhibiting these hormones
e..g ACh also stimulates gastrin and histamine as well as direct actions
e..g. S cells in duodemum secrete secretin which inhibits gastrin by G cells
e.g. D cells produce somatostatin which inhibits gastrin
e.g. acidity itself inhibits gastrin - negative feedback
describe the control of pepsin release
pepsin is an enzyme responsible for hydrolysing peptide bonds in proteins.
pepsinogen is secreted by cheif cells and then converted to active pepsin by stomach acid
pepsinogen secretion is stimulated by… low pH, gastrin, vagal stimulation
what stimulates gastic mucus production?
vagus nerve
gastrin
prostaglandins
what is the role of prostaglandins in gastric mucosa?
stimulate mucus and HCO3 production - protects stomach lining from acid
improves blood flow to mucosa
what happens if the balance between acidity and mucus is lost in the stomach?
mucosal surface irritation - gastritis
ulceration
what is the role of H.pylori?
stimulates gastrin release
produces ammonia which damages cells and reduces mucus production
what are the 3 phases of gastric secretion?
cephalic
gastric
intensitinal
cephalic
* anticipation of food - vagal nerve stimualtion - gastrin, histamine release, direct acid production, gastric motility
gastric
* presence of food, stomach distension
* i.e. stretch receptors - more vagal stimulation
* peptides stimulate gastrin production
* at pH less than 2 somatostatin released as negative feedback
intestinal
* chyme enters intestine - acidity - negative feedback by 3 main hormones.
* secretin = inhibit gastrin
* gastrointestinal peptode = inhibits gastrin
* Cholecystokinin (CCK) = inhibits stomach emptying
* also promotes pancreatic enzyme release
what is the difference between reflux, aspiration and regurgitation
reflux = from stomach up oesophagus
regurgitation = into oropharynx
aspiration = into lungs
what are the functions of the stomach
main role in digesting and churning food to create chyme that can be further handled by the intestines
food storage
absorption - some drugs e.g. alcohol, aspirin
immune role - acidity kills microbes
intrinsic factor - absorption of B12
describe the function of intestinal hormones acting on the stomach
Secretin = S cells - stimulated by acidity of chyme, inhibits gastrin
CCK = I cells - stimualted by aa and fats - stimulates pancreaes and inhibits gastric emptying
gastrointestinal peptide = K cells - stimulated by fatty acids in small intestine, reduces emptying and gastric juice production. stimulates insulin
Somatostatin = D cell
what are the sphincters in GIT?
Upper oesophageal
lower oesophageal
pyloric
ileocaecal
sphinchter of oddi
anal
tell me about the oesophageal sphincters..
2 of these
upper and lower
upper - under somatic control. made up of cricopharyngeal part of inferior pharyngeal muscles
lower - under autonomic control. remains contracted at rest with a pressure of around 15-20mmHg. during swallowing the stretch of the oesophagus stimulates vagus to cause relaxation .
what is meant by the oesophageal barrier pressure?
the barrier pressure is the difference between gastric pressure and LOS pressure.
LOS = 15-20mmHg
gastric pressure normally lower at rest
hence barrier pressure is LOS - GP which is positive at rest.
if LOS reduces or gastric pressures increase the barrier pressure can drop resulting in reflux.
what factors influence reflux
barrier pressure = LOS - gastric pressure
reduced LOS = anaesthetic agents, alcohol, oestrogen/progesterone (pregnancy), antimuscarinics. physiological factors - swallowing, vagus nerve
increased gastric pressure = full stomach, pregnancy, bowel obstruction, obesity. delayed emptying (opioids, pain)
babies have low LOS and high gastric pressure hence reflux
what factors increase LOS tone?
cholinergic stimulation - neostigmine, cyclizine, succinylcholine
describe the control of gastric emptying?
stomach emptying occurs when pressure created by stomach pump exceeds pyloric pressure
in general, gastric emptying is proportional to fullness of stomach i.e. fuller, the quicker
howeveer there are a number of neural and hormal factors influencing this…
neural = enterogastric reflex
* food in duodenum - walls stretch - vagus nerve inhibited - reduces motility , slows emptying.
* gives time and control over emptying
hormonal =
* chyme + acidity in duodemum, release of CCK and secretion - reduce motility
External
* prokinetics (erythomycin, neostig, metoclop)
* opiods
* pain, fear - reduces
how does the stomach breakdown food?
mechanical - churning
chemical - pepsin, acidity
describe the process of swallowing..
both a voluntary and involuntary process
1. voluntary movement of food bolus to posterior mouth. sensory afferents via trigeminal, glossopharyngeal and vagus to swallowing centre
2. causes brainstem activation of swallowing stages. elevation of soft palate to close off nasopharynx
3. closure of vocal cords and larynx drawn down. epiglottis swings over cords. upper oesophageal spinchter widens
4. peristasis starting in upper oesophagus - coordinated by swallowing cells (medulla and pons). swallowing centre inhibits resp centre. LOS relaxes.
describe the breakdown of macromolecules
carbohydrates - amylase in saliva and pancreatic juices. makes oligosaccharides and disaraccharides. further broken down by lactase, sucrase and maltase into glucose which can be absorbed.
proteins = pepsin and aa are absorbed
fats = lipase and emulsification
describe the breakdown and absorption of fats by intestines..
lipids are emulsified by bile salts
increases S.A for lipase to breakdown triglycerides to FFA and glycerol
FFA, cholesterol, fat soluble vitamins and other molecules form micelles
at the luminal membrane, FFA and monoglycerides leave the micelle and are absorbed into intestinal cell.
within intestinal cell, they reform to form chylomicrons
chylomicrons enter lymphatics via exocytosis
enter blood at thoracic duct
capillary endothelium has lipoprotein lipase which further digests and allows uptake of FFA to cells.
chylomicrons with removed FFA return to hepatocytes
how is glucose absorbed from GIT?
secondary ATP
Na/K ATPase on basolateral membrane
gradient for NA into the cell
SGLT 2 = cotransport for Na and glucose - luminal
GLUT 2 = basolateral
define nausea
define vomitting
nausea - unpleasant experience / senation of the need to vomit
vomitting - physical involuntary forceful expulsion of gastric content via the mouth
describe the physiology of vomiting..
complex process involving many afferent and efferent pathways
Thought to be coordinated by the vomitting centre - an area within the medulla oblongata made of multiple neural connections.
This recieves 3 main inputs
* chemoreceptor trigger zone - lies at base of 4th ventricle, area postrema and lies outside of BBB allowing it to sense toxins within the blood and input into vomitting centre
* nucleus tractus solitarus - lies within medulla - recieves inputs from various areas (vestibular apparatus, GIT, pain afferents)
* higher centres - pain, emotion, fear, raised ICP
various neurotransmitters and receptors are involved including dopamine, serotonin, acetylcholine, histamine and mu opioid receptors.
once threshold reached, central pattern generator activated and vomitting initiated.
describe the vomitting reflex..
pre-ejection - nausea, activation of sympathetic NS - sweating, tachycardia. also parasymp - salivation, relaxation of oesophageal sphincters and retrograde peristalsis
retching - respiration caeses, glottis closes, larynx rises, soft palate elevates - protect airway
ejection phase - coordinated contraction of diaphragm and abdominal muscles.
can you tell me some stimuli for vomitting?
toxins in blood - CTZ - many receptors D2, 5HT3, u opioid, neurokinin (sub P)
vesticular apparatus - motion sickness - via H1 and M3 reecptors
GIT - toxins in gut lumen, gut visceral pathology - 5HT3, dopamine receptors and substance P all implicated. e.g. 5HT3 receptors on end of vagal afferents which transmit impulses to vomitting centre.
raised ICP
complications of vomitting
electrolyte disturbance
dehydration
aspiration
poor absorption/ malnutrion
increase ICP
wound dehiscence
what are the risk factors for PONV?
patient factors - anxiety, female, previous PONV or motion sickness, non smoker, dehydration
anaesthetic factors - inhalation agents, N20, opioids . over use of bag/ mask ventilation and stomach inflation
surgical factors - obsteric, cholecystectomy, middle ear , laparoscopic
how does PONV in children compare to adults?
increases with age - more likely than adults
rare under 2
no sex differences before puberty
do you know any scoring systems for PONV?
APFEL
* adult scoring system
* 1 point for each = female, non smoker, opioids, prev PONV
* each point = 20%
POVOC
* paediatric tool
* 1 point = op more than 30mins, stradbidmus surgery, prev PONV, FHx PONV
describe the microscopic structure of the liver…
made up of millions of lobules
Whereby there is a branch of the hepatic vein at the centre of a hexagonal structure
at each corner of the hexagon is the portal triad = hepatic artery, portal vein, bile duct
30% of blood flow is via hepatic artery and 70% via the portal vein
however hepatic artery and portal vein supply around 50:50 of O2 content to the hepatocytes - they drain into sinusoids which lie between the hepatocytes. these sinusoids eventually meet and drain into the hepatic vein.
bile duct cannuli also line the hepatocytes, which make bile which is drained via bile duct
the liver can also be divided into zones 1,2,3 - this is a functional division (acinus) - zone 1 is closest to arteries and zone 3 closest to hepatic vein.
what is the difference between hepatic lobule, acinus and portal lobule
liver acinus = functional unit
describe the structure of hepatic sinusoids
hepatic artery and portal vein empty into the sinusoids - capillaries which pentrate hepatocytes and drain into hepatic vein.
large gaps (sinusoidal cap) to allow passage of proteins and sometimes cells
close association with kupffer cells
what is the cori cycle?
the metabolic pathway of conversion of lactate back to glucose during aerobic conditions
during anaerobic exercise, lactate can build up from glycolysis. (produced by lactate dehydrogenase). this also occurs in ischaemia or all the time by RBC (no nucleus)
the lactate is transported to the liver in the blood and converted back to pyruvate and then glucose - for further glycolysis, glycogen storage or production of aa.
certain lactate dehydrogenase isoenzymes can catalyse the reverse reaction
how does the body handle starvation..
starvation is defined as the failure to ingest sufficient calories to sustain normal body function
during starvation - blood glucose needs to be maintained for RBC and brain
this is via gluconeogenesis due ot fall in insulin, rise in glucagon
slowly levels of FFA and ketones rise as fats are metabolised and ketosis takes place..
first 24 hrs = glycogen stores used. glucose drops iniitially, causes increase glucagon, drop in insulin. promotes glycogenolysis
day 1 -4 = glycogen depleted, glucose levels stabilised. fat metabolism predominates. FFA and glycerol produced. FFA can be used by non-glucose dependant tissues. glycerol converted to glucose by gluconeogenesis.
day 4 plus =
FFA are converted to ketones (ketosis)
brain adapts to use ketones
