Introuduction To The Stomach Flashcards
Describe the journey of hormones secreted from endocrine cells to their target location?
Peptides released from endocrine cells
Pass into portal circulation (portal vein)
Through liver
Systemic circulation (IVC, aorta, Celiac/ superior mesenteric/ IM)
Back to near where they were secreted
What is a paracrine hormone, give an example?
Relating to a hormone which has effect only in the vicinity of the gland secreting it
E.g. acid in antrum stimulates somatostatin release(D cells) to inhibit gastrin secretion(G cells)
What is neurocrine secretion, give an example?
Peptides released by neurones after AP
E.g. sight of food/ chewing -> gastrin releasing peptide (post-ganglionic fibres vagus N) increases gastrin release(G cells)
What are the two broad categories of gastrointestinal hormones and give two examples for each category?
Gastrin family:
- Gastrin (G cells antrum of stomach)
- Cholecystokinin (I cells duodenum/gallbladder)
Secretion family:
- secretin (s cells duodenum)
- gastric inhibitory polypeptide (duodenum & jejunum)
What is gastrin? Where is it secreted and what is it’s function? What stimulates its release?
A gastrin hormone
G cells antrum stomach
Increases gastric acid secretion
Stimulated by: peptides/ AAs in stomach, vagal stimulation of Ach , gastrin-releasing peptide
What is cholecystokinin? Where is it secreted, what’s its function and what stimulates its secretion?
gastrointestinal gastrin hormone
I cells duodenum and jejunum
Increases pancreatic and gallbladder secretions
Stimulated by fat and protein
What is secretin? Where is it released? What is it stimulated by? What it’s function?
Secretion hormone
S cells duodenum
Stimulated by H+ and Fa
Increases HCO3 (bicarbonate) from pancreas/ gallbladder ~ neutralises acidic chyme entering duodenum from stomach (also made in RBC/ PCT/ DCT compensatory mechanism) & decreases gastric acid secretion
What is gastric inhibitory polypeptide? Where is it secreted, what stimulates it and what is it’s function?
A gastrointestinal secretin hormone
Cells in duodenum and jejunum
Stimulated by sugars, aa, fa
Increases insulin and decreases gastric acid secretion
Main functions of the stomach
Short term storage food
Vigorous contractions of smooth muscle to increase SA food
Continue digestion - swallow amylase/ lipase, add proteases
Disinfect- acidity/ enzymes
Activate (renature) proteases
Chief cells in gastric glands-> Pepsinogen (activated by HCl)-> pepsin
Anatomy of the stomach, areas, curves and sphincters
Fundus- top
Cardia- near oesophagus entrance (above heart)
Body- main part
Antrum- end
Greater (lateral) and lesser curve (medial)
Lower oesophageal
Sphincter
Pylorus sphincter into duodenum
Rugae - mucosal and submucosal folds increase SA
Many little holes - gastric pits with gastric glands below
Epithelium of the gut
Stratified squamous in oesophagus and distal anus, everything between is simple columnar
Stratified squamous is more protective against abrasion
Types of epithelium cells in the stomach and their function
Other cell types in the stomach and their function
All simple columnar
Mucous cells- mucous lines stomach under acid layer
Parietal cells- secrete HCL and intrinsic factor (absorption V12)
Chief cells- proteases (pepsinogen and chymosin)
G cells- gastrin
Inferior to epithelium:
Enterochromaffin like cells- histamine (induces production of gastric acid)
D cells -> somatostatin (inhibits G cells)
Name of the stomach smooth muscle and function
Extra oblique layer of muscle
Mix/grind contents
Move contents along
Compare stomach contractions in the upper and lower stomach? How does the shape of the stomach aid movement of contents? How often is chyme ejected and where?
Upper- sustained contraction which create basal tone
Lower- strong peristalsis mixes contents, coordinated movements, contractions every 20seconds proximal to distal
Stomach is larger proximally so contents are accelerated and lumps left behind
Liquid chyme ejected into duodenum 3 times a minute
Branches of the coeliac trunk
Coeliac trunk (first branch of abdominal aorta)
- > left gastric
- > splenic: -> superior aspect pancreas, short gastric, left gastroepiploic
- > common hepatic (-> gastroduodenal -> anterior superior pancreaticoduodenal + right gastroepiploic) -> proper hepatic -> left hepatic + right hepatic -> cystic
Look in notebook
Abdominal aorta branches
Superior-> inferior
Coeliac trunk (foregut)
Superior mesenteric artery (midgut)
Testicular/ ovarian
Inferior mesenteric (hindgut)
Bifurcation:
Left common iliac-> external & internal
Right common iliac -> external & internal
Venous drainage of the foregut, midgut and hindgut
ALL drain into portal vein which drains into IVC
Foregut veins -> portal
Midgut-> superior mesenteric -> splenic vein -> portal
Hindgut -> inferior mesenteric -> portal
Venous drainage of the stomach
Right gastric
Left gastric
Middle gastric
-> portal
Short gastric Left gastroomental Right gastroomental -> superior mesenteric vein -> portal
What is receptive relaxation of the stomach and why does it need to occur?
Receptive relaxation of fundus of stomach as food enters through the distal oesophageal sphincter vagally mediated
Allows food to enter without raising intra-gastric pressure too much and prevents reflux
Gastric mucosa folds (rugae) allow distension
What cell type predominantly makes up the cardia?
Mucous cells
What cell types predominately make up the fundus & body and so what secretions?
Mucous cells
Parietal cells -> HCL
Chief cells -> pepsinogen
What cell types predominately make up the pylorus and so what secretions?
G cells -> gastrin
D cells -> somatostatin
What are the 3 stimulants of the parietal cell to secrete H+?
G cells (sight/ smell of food/ stretch/ peptides or AA from stomach lumen) -> gastrin though CCK channel
Entero-chromaffin like cells -> histamine through H2 channel (amplifies gastrin)
Parasympathetic vagus Nerve-> signal
What happens once food leaves the stomach to turn off the digestive mechanisms?
Food acts as a buffer so once it leaves the PH drops
This activates D cells to secrete somatostatin which inhibits G cells and entero-chromaffin like cells
What is the ‘alkaline tide’ and what is it’s function?
Durin HCL poorudction parietal cells extract CL-, CO2, H2O & Na from blood plasma
After eating partial cells secrete HCO3- bicarbonate through their basolateral membrane into the blood to maintain the electrical balance
Lasts until acids in food absorbed in the small intestine reunite with the bicarbonate (usually under 2 hours)
Explain how HCl is produced in parietal cells
Anion antiport protein on basolateral membrane - Cl- in and HCO3- out
Cl- transcellular diffuses to Cl- channel protein on apical membrane
CO2 diffuses through basolateral combines with OH- from H2O to form HCO3- (which antiport with CL-)
H20 also produces H+ which goes through H+/K+ ATPase on apical membrane
(k+ channel protein apical where K+ diffuses out to create concert grad)
Slide 30
What are the 3 stages of digestion and what percent is each responsible for total HCL production?
- Cephalic- 30%
- Gastric - 60%
- Intestinal - 10%
What stimulates the cephalic phase of digestion and what does it cause?
Parasympathetic stimuli e.g. smell/ taste/ chewing/ swallowing
Direct stimulation of parietal cells by vagus Nerve
And G cells by vagus (GRP released)
Also slightly increases gastric motility
What occurs in the gastric phase of digestion?
Distension of stomach stimulates vagus -> stimulates parietal and G cells
At this stage food is acting as buffer so gastrin is not inhibited
Enteric Ns and gastrin cause strong smooth muscle contractions
What occurs in the intestinal phase of digestion?
Chyme initially stimulates gastrin secretion
Partially digested proteins detected in duodenum
Short Phase as soon overtaken by inhibition of G cells
Presence of lipids activates enterogastric reflux (stretching wall duodenum) -> Reduces vagal stimulation
Chyme stimulates CCK and secretin (helps suppress HcL secretion)
How does the stomach protect itself from self-digestion?
Foveolar cells secrete mucin which forms a viscous mucus layer that adheres to epithelium and prevents physical damage from food
HCO3 ions are secreted into mucus to provide a neutral barrier against the stomach acid
Rich blood supply to gastric mucosa can remove and buffer acid that has breached the mucus layer
Prostaglandins promote above processes
High turnover of epithelial cells to remove damaged cells
Inactivation of proteases
Parietal and G cell inhibition when food has left
Why should you eat before taking NSAIDS?
Decrease prostaglandin release which promotes protective process for the stomach e.g HCO3/ mucus secretion
If not could get a stomach ulcer and bleed
Name some damaging factors to the stomach
H+
Pepsin
H.Pylori-> chronic active gastritis -> ulcers (1/2 of us have in normal flora)
NSAIDs inhibit prostaglandins
Physiological Stress (3rd degree burns/ head trauma)
Smoking
Alcohol dissolves mucus layer -> gastritis
