GI - Stomach Flashcards
Important Anatomy of the Stomach
Cardiac Sphincter (physiological sphincter)
Fundus
Cardia
Body
Pyloric Antrum
Pyloric Canal
Pyloric Sphincter (anatomical sphincter - thick SM)
Lumen
Angular Notch (Start of the pyloric Region)
What is the importance of the cardiac sphincter?
- start of the oblique layer of muscle
- Area of the intrinsic and extrinsic lower oesophageal sphincter
Where do the greater and lesser omentum attach?
Lesser Omentum - Lesser Curvature
Greater Omentum - Greater curvature
What is the importance of the arrangement of blood vessels of the stomach?
Anastomoses allows the stomach to move as diaphragm moves up and down
What Glands are found in the regions of the stomach, and what is the main role of these regions?
Fundus - Fundic/ Oxyntic Glands. Release HCl and Pepsinogen - Digestion
Cardia - Cardiac Glands. Protection - Produce Mucus
Body - Fundic/ Oxyntic glands. HCl and Pepsin - Digestion
Pyloric Antrum - Pyloric Glands. Produce Mucus, gastrin, somatostatin. Regulate acid production
What is the pyloric sphincter a Landmark for?
The trans-pyloric plane (in X-rays)
Blood supply to the Stomach?
Short Gastric A (from splenic)
Left Gastric A Left Gastroepiploic A
R Gastric A R. Gastroepiploic A
Gastroepiploic - from splenic or Gastroduodenal
L gastric - from cephalic trunk
R gastric - from hepatic
All drain to portal vein system
Special histology of stomach
- simple columnar epithelia
- Mucosa in rugae
- Gastric pits extending to lamina propria, with glands at the bottom
submucosal plexus - secretory cell control
Muscularis externa - longitudinal, circular, oblique
Myenteric plexus between longitudinal and circular - controls motility
Mesothelium (simple squamous) around serosa - peritoneal lining
Secretory cells in Different Glands of stomach
Fundic/ Oxyntic Glands - Parietal cell (HCl), Chief cell (pepsinogen), some G cells (Gastrin) and ECL (histamine) cells.
Cardiac- surface epithelium and neck cells - both produce mucus
Pyloric - mucus secreting cells, G cells and D cells
Position of secretory cells in glands
Mucus Neck cells - top of gastric gland Parietal cells - next Chief cells - next ECL Cells - bottom Gastrin - Bottom
Innervation of Stomach
Parasympathetic - Vagus nerve. Increase secretion/ motility of stomach
Sympathetic - thoracolumbar. Decrease Secretion/Motility.
Connect to ENS or directly to smooth muscle or gland.
Parietal Gland - Function, Histology
- Produces HCl and IF
- Activates pepsinogen
- kills microbes
- denatures proteins
Highly regulated
Structure
- Many mitochondria - must lower lumen from pH8 -> pH2
- Caniculli for proton pumps to release H+ in to
Mucus production - cells and function
Mucus -
- protective (1mm surface, bicarb)
- lubricate
- neck cells and surfae epithelium
Chief cells - Histology and Function
Release Pepsinogen (zymogen) - Regulated similarly to HCl Activated by pH 0.8-3.5 Endopeptidase Irreversibly inactivated in duodenum Digest 20% protein
What ions are released to the stomach by parietal cells and how?
K+, H+, Cl-, H2O
Make H+ by splitting Water
- OH joins CO2 from blood to make HCO3, which is antiported to blood for CL
H+ enters lumen through H+/K+ ATPase antiporter
Cl to lumen through channel
K+ to lumen through channel, from blood through K+/Na+ ATPase antiporter
H2O diffuses across
Histamine - cell, receptor, what stimulates release, what inhibits
Cell - ECL cells
Receptor - H2 receptor on parietal cell
Stimulated by: Ach
Inhibited by: SST
Gastrin - cell, receptor, what stimulates release, what inhibits
Cell - G cell Receptor - CCK 2 on parietal cell Systemically released Stimulated by: raised pH, GRP (from PS neurons), directly by proteins/distention, Inhibited by: Secretin, lowered pH, SST
Somatostatin- cell, receptor, what stimulates release, what inhibits
Cell - D cell
Receptor - SST receptor on parietal cell
Inhibits Gastrin, Histamine, Secretin, CCK release
Stimulated by: Gastrin, secretin, lowered pH
Inhibited by: ACh
What makes up the gastric barrier? What damages it?
TJs and surface mucus
Aspirin and Alcohol damage GB through mucosal damage
Regulation of Gastric Secretion - stimulators and inhibitors
Stimulators
- Gastrin
- Histamine
- ACh
Inhibitors
- Somatostatin
- Secretin (Acid/ Fat)
- Low pH
- CCK (FA/ AA)
- GIP (FA and AA)
What are the 3 Gastric Acid Phases
Cephalic, Gastric and Intestinal
Describe the role of the PSNS in gastric secretion of the stomach - cells act on, nerve, receptors, what it stimulates to be released
Vagus innervation - Long vasovagal reflex
ENS - short reflex
acts on M3 Receptors - Parietal cells, chief cells and mucus cells
- Gastric Secretion and Gastric Emptying
What effect does lowered pH have on the stomach?
Inhibits gastrin directly
Stim somatostatin
Occurs 1 hr after digestion
Secretin - cell, receptor, what stimulates release, what inhibits
Cell - S cells (neuroendocrine cell in intestine)
Function: Increase pepsin secretion, decrease acid secretion and gastrin secretion, increases SST increases bicarb production in biliary system and pancreas
Stimulated by: Acid, Fat
Inhibited by: SST
CCK - cell, receptor, what stimulates release, what inhibits
Cell - I cells (NEC in SI)
Function
- Increases contraction of the gall bladder, exocrine secretion of pancreas
- Decrease appetite (Vagus afferents) and Gastric emptying
Stimulated by: FA, acid, AA
Inhibited by: SST
GIP- cell, receptor, what stimulates release, what inhibits
Cell: K cells in upper intestine
Function: decrease gastric emptying and increase insulin production
Stimulated by: FA and AA
Inhibited by:
Describe the cephalic phase
Stimulated by sight/ smell/ taste/ thinking of food
- Vagus innervation
from cerebral cortex and appetite centers of amydala/ hypothalamus - ACh release: Gastrin, Histamine, Acid release and pepsinogen release
Moderate stimulation = 30% Acid released
Describe the Gastric Phase
Stimulated on protein detection and distention
- Mechanoreceptors and chemoreceptors triggered, by stretch and proteins.
- Cause vasovagal long reflex and ENS short reflex
- Release of HCl, Gastrin, Histamine and Pepsinogen
2 Gastrin triggered by proteins/ peptides/ coffee/ Ca
- Food neutralises HCl = increases pH
Increases Gastrin and Histamine
60% acid secretion
Describe the Intestinal phase
Food in duodenum
Presence of Acid/ Distention/AA/ FA
Acid = Secretin
- increases SST, decreases Gastrin and Acid secretion in stomach = Less Acid
Lipids/ FA/ AA= CCK
- Less gastric emptying and appetite
- increase gallbladder and pancreatic exocrine secretions
Lipids/ FA/ AA = Peptide YY
- Less gastric emptying and appetite
- increased water and electrolyte absorption
AA/ FA = GIP
- less gastric emptying
- increased insulin
What stimulates gastric emptying
stretch - mechanoreceptors
proteins - chemoreceptors
= Parasympathetic reaction - long and short reflexes
How does the vasovagal reflex work? what cells does it work on?
Controlled by the medulla
Signals through vagus nerve
Causes ACh release
Acts on SM pacemaker cells (Cells of Cajal) in the longitudinal muscle
Cells of Cajal control the BER of the stomach (3 depol/repol waves per minute) - these are quite weak
Increased AP frequency (in response to signals) = increased chance of reaching threshold for AP signal = stronger contractions
Causes Receptive relaxation of stomach
What is the result of the parasympathetic nervous system on gastric emptying?
Stomach Relaxation - Receptive relaxation in body and fundus ( allow storage of food)
Peristaltic Waves from pyloric Antrum
What causes stomach relaxation?
Short ENS reflexes cause ACh release (also long VV reflex)
Causes NO and Serotonin release
Receptive relaxation of fundus and body (Increased volume with no increased pressure)
How does it travel from longitudinal to circular layer
GAP junctions to circular layer and rest of the stomach
Mechanical digestion in the stomach
Churning motions - mix luminal contents
Retropulsion against the closed pyloric sphincter (closed in contractions) - force of food disperses chyme
to get to duodenum must be liquid
Regulation of the Basal electrical rhythm
Neural and Hormonal stimuli = increase AP to reach threshold = increased strength contraction
Fasting BER is weak
+ Gastrin (increase force and movement)
+ PS stimulation
- increased acidity (secretin) / distention (CCK) / AA (CCK)/ FA in duodenum
- Peptide YY, GIP
- Hypertonic Solution
- Sympathetic stimulation
Receptors on parietal cell and result of binding
Cause Ca release = expression of H+/K+ ATPAse on cell surface
- M3 - Ach
- CCK2 - Gastrin
Effects cAMP through GPCR
- H2 - Histamine, cause cAMP prod and expression of H+/K+ ATPAse
- SSTR - inhibits cAMP through AC
What is a peptic ulcer and where are they commonly found
Ulcer caused by the action of pepsin and stomach acid - causes mucosal damage through increased acid production (usually) and erodes away stomach/ duodenum
Commonly found in stomach. More commonly in duodenum - undergoes metaphasia to stomach columnar cell in response to increased acid, then gets ulcer.
RF for Peptic Ulcer and causes of Peptic Ulcer
RF
- Male
- Smoker
- Stressed
- increased acid production
- Diet
- Alcohol
- Aspirin/ increased NSAIDs
- Caffeine
Symptoms of Peptic Ulcer
Pain, particularly after meals Reflux is other common side effect of increased acid weight loss Nausea/ vomiting Bloating Easily full Heartburn
Erodes to hit major BV = haemorrhage and vomiting blood (haematymysis)/ occult stool
Erode all the way through = acute peritonitis (patient will collapse)
Only treatment is surgery here
Pathophysiology of peptic ulcers
Usually caused by H. pylori
H. pylori
- makes urease, converts urea to ammonia to regulate pH to allow it to survive in stomach
- if colonises antrum, alkaline cloud covers G cells and D cells, preventing low pH detection and SST release from D cells
- unregulated increased Acid production - increased risk acid in duodenum and increased risk ulcer.
Increased Duodenal Acid load
- increased gastric metaplasia and H. pylori infection and ulceration of duodenum
-H pylori infection causes gastritis, can also cause D cell atrophy = less somatostatin
More prevalent in Cag +ve individual (more westerners) = more inflammation
List Treatment of peptic ulcer
Surgical
- Vagotomy, Subtotal gastrectomy, anterectomy
Medical
H2RA - block H2R
PPI - Act directly on parietal cells
- not good, control not cure and expensive
Sucralfate and bismuth salt seem to be curative
AB for H pylori infection is most effective treatment
Treatment for H. pylori infection
First Line: Omeprazole, metronidazole and amoxycillin
2nd Line: OP, amoxycillin and clarythromycin
Allergy to penicillin and Clarythromycin
Diagnostic tests for Peptic ulcers and H pylori infection
Urea Breath Test- urea labelled with C13/ C14 - in 10-30 mins test to see if radiolabelled CO2 breathed out
Urease Slide test
- biopsy of mucosa in gastroscopy and then CLO test ( urea to see if urease converts to NH3 and CO2) pH indicator phenyl red turns red if present
Blood - Antibodies Foecal - antigens - Urine Endoscopy and biopsy - microscopy - serology - culture
Pathophysiology of H. pylori infection causing gastric cancer
Presents with - weight loss, anorexia , anaemia and usually uncurable
Mostly attributed to H pylori (some to AD genetics condition)
If infection at bottom of stomach
- inflammation can cause atrophic gastritis (G cell atrpohy = less gastrin = less acid - hypochlorohydria
- Chronic atrophic gastritis
- metaplasia that becomes dysplastic
Summary: H pylori → superficial gastritis → (mediated by host genetics, bacterial strain + Environmental factors) atrophic gastritis + hypochlorhydria → (Mediated by gender + Environmental factors) Dysplasia + Cancer.
Risk high in China and Japan
If get peptic ulcer, less likely to get H pylori mediated gastric cancer
Epidemiology of peptic ulcer disease
Related to socioeconomic conditions as kid (where get H pylori infection) younger kis are much less likely to have infection now than older.
Protective function of H pylori infection
Raises pH of in stomach in general population, especially as people age and secretory cells get less effective anyway = protective for GORD and oesophageal cancer
