5. GORD Flashcards
GORD
Gastroesophageal reflux disease
Q Describe the anatomy of the upper GI tract including the course through the thoracic cavity
(pharynx, oesophagus, stomach and
duodenum)
Upper oesophageal sphincter formed by the cricopharyngeus muscle (part of the inferior pharyngeal constrictor)
Lower sphincter – contributed by the crura of the diaphragm, a ring of smooth muscle in the oesophagus and pressure differences in the abdomen and thorax (a structure of combined features – not a single anatomical structure)
Physiology of swallowing:
- Voluntary contraction of the pharynx
- Upper oesophageal sphincter opens
- Reflexes stimulated by pressure receptors in the walls of the pharynx
- This sends impulses to the swallowing centre in the medulla
- Causes the elevation of the soft palate (uvula)
- Blocks off the nasal cavity to stop food going into the nose
- Swallowing centre inhibits respiration
- Rimaglottidis close (space between vocal cords)
- Larynx raises up
10.Epiglottis closes the laryngeal inlet - Food moves down the pharynx – constrictor muscles contract in sequence to push the food
down - As soon as the food passes through the upper oesophageal sphincter, it contracts
- The Rimaglottidis then opens and breathing resumes
- Food moves down the oesophagus by peristalsis and reaches the stomach in 9 seconds
- Lower oesophageal sphincter is open throughout
- Closes as soon as food enters the stomach to prevent reflux
Blood supply to oesophagus
- Upper 1/3 – inferior thyroid arteries
- Middle 1/3 – branches from the abdominal aorta
- Lower 1/3 – oesophageal branches from the left gastric artery
Blood supply to the Salivary glands
- Parotid – serous only – Stenson’s duct
- Sublingual – mucus only – Wharton’s duct
- Submandibular – mixed – Wharton’s duct
Q Describe the physiology of gastro-oesophageal motility and reflux
Enteric nervous system – pacemaker 3/min, cells in the longitudinal (interstitial cells of Cajal)
Oesophageal motility – peristalsis
Stomach – receptive relaxation
Stomach motility
Wave of depolarisation from the fundus to the body
Reaches the muscle mass of the abdomen and causes retropulsion by closing the pyloric sphincter to mix the chyme
A small bit of chyme will enter the duodenum with each contraction
As gastrin concentration increases, the strength of contraction increases
Gastric emptying – rate becomes controlled by the duodenum
Factors that increase emptying
gastric distention, gastrin, increased osmolarity and peptides and fats in the stomach, parasympathetic stimulation
Factors that decrease emptying
- duodenal phase – duodenal distention (decreases parasym, to stomach, detectedby duodenal stretch receptors), presence of fats – causes release of CCK from the duodenum, CCK amplifies secretin. Secretin release also caused by presence of acid in the duodenum. Secretin then inhibits gastrin and histamine to reduce acid production and gastric emptying.
Q Describe the physiology of acid production in the stomach
Stimulated by 3 main factors – gastrin (G cells), acetylcholine (parasympathetic neurones), histamine (ECL cells)
Inhibited by – somatostatin (D cells) inhibits al of the stimulating factors
Act on parietal cells to cause the release of H+
Secretin – released in response to low duodenal pH. Inhibits gastrin, promotes somatostatin
CCK
Phases of gastric acid production
1. Cephalic phase - Site, smell and anticipation of food causes parasympathetic stimulation
2. Gastric phase “turning it on” – gastric distention (stretch receptors cause acetylcholine
release), distention also causes the release of gastrin from G cells by physical stretching of the gastric pits. These 2 factors then act on the ECL cells to cause them to produce histamine.
3. Gastric phase “turning it off” – high levels of acid in the stomach (low pH) stops gastrin
and promotes somatostatin release. This then decreases acid production from parietal cells as there is a lack of stimulation from gastrin and inhibition on every single stimulating factor by somatostatin.
4. Intestinal phase “turning it off” – duodenal distention – decreases parasympathetic
stimulation to the stomach which means less ACh released. Presence of acid in the duodenum causes the release of secretin from enterocytes. Secretin directly inhibits gastrin and promotes somatostatin. Fats presence causes CCK release, which decreases gastric emptying and gastric acid production by
Q Describe the defences of the gastric and duodenal mucosa against acid damage
- Tight junctions in the epithelium to prevent acid leakage
- Mucus production (alkaline pH)
- Feedback loops – the fact that acid inhibits gastrin and promotes somatostatin
- Enzymes release as zymogens
- Prostaglandins involved in mucus production
- Stem cells at the bottom of the pits, migrate vertically to replace the cells at the top every few days (the cells that are replaced horizontally are smooth muscle and bone)
Describe the key features of a history of reflux and dyspepsia
Barratt’s oesophagus – when the oesophageal epithelium (stratified squamous) becomes gastric epithelium (simple columnar)
Common site for cancer and the initiation of cancer – as are all transitional epithelia
Reflux more common fat people, complain of pain at night, and describe the pain as indigestion (dyspepsia)
Red flag symptoms, differential diagnoses for cancer: weight loss, >50yr, bleeding etc
Could be due to weaknesses in the lower oesophageal sphincter, or acid XS.
F What is secreted by D cells?
a) Stomach acid
b) Somatostatin
c) Gastrin
d) Pepsinogen
e) Adrenaline
- ) Amylase
- ) Acetylcholine
- ) Glycogen
- ) CCK
- ) Saliva
- ) Chymotrypsinogen
b) Somatostatin
F What substance is secreted by Enterochromaffin (ECL) cells?
a) Histamine
F What substance is secreted by G cells?
c) Gastrin
F Which of these substances is secreted by Chief cells?
d) Pepsinogen
