GI S5 (Done) Flashcards
What mechanisms prevent gastric reflux?
Lower oesophageal sphincter (LES):
Usually closed, transiently relaxes to allow bolus through
Stomach:
Angle of His and mucosal flap valve, as well as the postero-lateral location of the fundus all prevent acid reaching the LES and refluxing
Diaphragm:
Right crus of diaphram acts as a sling around the oesophagus serving as an ‘extrinsic’ sphincter
The failure of anti-reflux mechanisms leads to what?
Prolonged contact of gastric juices with oesophageal mucosa
Gastro-oesophageal reflux disease and associated symptoms
What are the typical clinical features of Gastro-oesophageal reflux disease (GORD)?
Dyspepsia
Worsens on lying down, bending over or drinking hot drinks
What investigations are indicated by a history that leads you to suspect GORD?
No investigations done in typical clinical presentations
Only if worrying symptoms, such as dysphagia or hiatus hernia are suspected
Endoscopic investigation in this case
What are some of the risk factors for GORD?
Pregnancy or obesity
Fat, Chocolate, Coffee or Alcohol
Large meals
Smoking
Hiatus hernia
List lifestyle management techniques to prevent/treat GORD
Lose weight
Stop smoking
Reduce consumption of chocolate, coffee, alcohol, fatty foods
Outline the types of treatment available for GORD, including their mechanism and an examples of each type
Simple antacids:
Neutralises acid with a base
E.g. Calcium carbonate
Raft antacids (alginates):
Forms a protective raft that sits on top of stomach contents and prevents reflux
E.g. Gaviscon
PPIs:
Reduction of acid secretion by oxyntic cells
E.g. Omeprazole
H2 antagonists:
Blocks H2 receptor which reduces acid secretions
E.g. Ranitidine
What is a common complication of GORD?
Continual contact of gastric juices and oesophageal mucosa can lead to metaplastic change (Barrett’s Oesophagus)
What is Gastritis?
Chronic or acute inflammation of the gastric mucosa
Differentiate acute and chronic gastritis
Chronic:
Infection with H. pylori
Inflammatory changes to mucosa leadsing to atrophy and metaplasia (possible cancer)
Acute:
NSAIDs, Alcohol, Cocaine
Exfoliation of surface cells and decreased secretion of protective mucus
What are the common symptoms of gastritis?
Commonly asymptomatic
Symptoms when they appear include:
- Dyspepia (Pain/Discomfort)*
- Nausea*
- Vomiting*
- Haematemesis*
- Melena*
Outline the complications of Gastritis
Increases risk of Peptic ulcer disease
Chronic gastritis can cause hypergastrinaemia due to increasing gastrin release from G cells, this in turn can lead to Duodenal ulceration (DU)
Chronic Antral H. Pylori gastritis can lead to Gastric cancer and mucosa associated lymphoid tissue lymphoma (MALT Lymphoma)
How is gastritis diagnosed?
Endoscopy/Biopsy
Testing for H. Pylori
Blood test (Anaemia due to GI bleed)
Stool test (Blood due to GI bleed)
What types of drugs are used to treat gastritis?
Antacids
PPIs
H2 antagonists
General theme is reduction in acid secretion for promotion of healing
Antibiotics
E.g. Clarithromycin/Amoxacillin
Treatment of H. Pylori infection
What is peptic ulcer disease?
A break in the superficial epithelial cells down to the muscularis mucosa of either stomach (GU) or duodenum (DU)
Where are peptic ulcers commonly found?
GU:
Lesser curvature and antrum
DU:
Duodenal cap
Outline the most common cause of peptic ulcer disease
Give statisitics
NSAIDs:
Inhibit prostaglandins and reduce production of unstirred layer of mucus
50% of patients with long term NSAIDs have mucosal damage
30% when endoscoped have petic ulcer(s)
5% are symptomatic
1-2% have complications such as GI bleed
What is the prevlance of the different forms of peptic ulcer disease and how do prevalence rates vary across ages and countries?
DU in 10% adult population
GU is 2-3x less common (3-5%)
Prevalence is lower among younger adults and higher in older
Developing countries have increasing prevalence of NSAID associated DU and decreasing prevalence of H. Pylori associated ulceration
What are the clinical features of Peptic ulcer disease?
Reccurent, burning epigastric pain:
Worse at night and when hungry in DU
Relieved by eating
Persistent severe pain:
Suggestive of penetrtion of ulcer into other organs
Back pain:
Suggests penetration of ulcer in posterior stomach
Nausea and vomitting:
Less common
Weight loss and anorexia:
GUs only
Sudden haematemesis:
Asymptomatic patients can suddenly present with haematemesis when a blood vessel is erroded
What are the common investigations for suspected Peptic ulcer disease?
Investigation of H. Pylori infection
In 55+ patients or those with alarming symptoms an endoscopy can be done to exclude cancer
How is peptic ulcer disease managed?
Triple therapy:
PPIs
H2 antagonists
Antibiotics for H. Pylori (Clarithromycin/Amoxicillin)
If taking NSAIDs, review use and perhaps use alternatives
Prevention:
NSAIDs and PPIs used together if NSAIDs are long term
What are the complications of peptic ulcer disease?
**Haemorrhage of blood vessels: **
Haematemesis
Melena
Perforation:
More common in DUs, normally into peritoneal cavity
Gastric outlet obstruction:
Can be pre-pyloric, pyloric or duodenal
Occurs due to active ulcers w/oedema or due to healing of ulcer with associated fibrosis/scarring
Normally presents as vomiting without pain
Describe H. pylori bacteria
Gram negatic, Aerobic
Helical
Urease producing
Found in the mucus layer of the stomach or adhered to gastric mucosa
What is the significance of H. pylori producing urease?
Urease produces ammonia and CO2
Ammonia:
Used to neutralise surroundings and protect the bacterium
C13 Urea test:
C13 Urea can be ingested by the patient to test for H. Pylori infection
Urease breaks down C13 urea forming C13 CO2 which can be exhaled and detected
How does H. Pylori colonisation of the gastric mucosa cause disease?
Secretion of enzymes and other substances that damage mucosa:
Ammonia is toxic to epithelia
Vacuolating cytotoxin A disrupts tight junctions and leads to apoptosis
Phospholipases
Inflammatory response to bacterium (Inflammatory cells and mediators)
What are some of the diseases caused by H. pylori infection?
Chronic gastritis
Peptic ulcer disease
Gastric Cancers
MALT lymphoma
How does H. pylori colonisation in different areas of the stomach affect clinical outcomes?
Antrum predominant colonisation:
DU risk
Antrum and body colonisation:
Largely asymptomatic
Body predominant:
GU and cancer risk
How is a bacterium implicated only in the colonisation of the stomach cause DU?
Antral H. pylori infection leads to hypergastrinaemia and hence increased acid production from oxyntic cells
Duodenal cap is inflammed and damaged by excess acid and metaplasia can occur
H. pylori colonises inflammed duodenal cap
Duodenal immune response leads to duodenitis and development of ulceration which is common intermittent
How can we test for H. pylori infection?
C13 Urea test
IgG serum levels
Endoscopy:
Gastric biopsy taken and H. pylori detected by histology and culture
How is H. pylori infection treated?
Same as Gastritis, GU or DU with H. pylori being the cause
PPI, H2 antagonist, Antibiotics (Clarithromycin/Amoxicillin)
90% successful in treatment of H. pylori
Outline the progression of H. pylori induced disease thus describing how it can lead to gastric carcinoma
Initial H pylori infection leads to chronic non-atrophic gastritis
Multifocal atrophy develops and leads to metaplasia of the underprotected mucosa
Dysplasia develops from metaplasia and progresses to carcinoma
Factors involved in progression:
H. pylori virulence factors
Virulence associated host gene polymorphisms (genetic predisposition)
Dietary and environmental factors alter progression
Why is gastric cancer a particulalry deadly cancer?
Mildly symptomatic/Asymptomatic until late stage
5-6th biggest cause of cancer death
Outline the mechanisms of drugs which reduce gastric acid production
PPIs:
Prevents H+ ions from being pumped into oxyntic cell canaliculi
H2 antagonists:
Removes amplification of the Gastrin/Ach signal for acid production
Describe the gross anatomy of the stomach
Expanded part of the GI tract between the oesophagus and the duodenum
2-3 litres in capacity
Resembles letter J
Position depends on posture, body shape, distention
5 parts:
- Body*
- Cardia*
- Fundus*
- Pyloric canal*
- Pyloric antrum*
2 Curvatures, greater and lesser
Label the diagram
Horizontal boxes, top to bottom:
Cardiac notch of stomach
Fundus
Cardia
Body
Pylorus
Antrum
Diagonal boxes, left to right:
Lesser curvature
Greater curvaure
What are the sphincters of the stomach and where are thy found?
Inferior oesophageal sphincter:
Found immediately superior to Z-line
In horizonatal plane with xiphoid process to the left of T11
Pyloric sphincter:
At the pyloric end of the stomach
Describe the structure and function of the inferior oesophageal sphincter
Immediately superior to the Z-line the diaphragmatic musculature forms the oesophageal hiatus
This functions as a physiological sphincter
Contracts and relaxes to allow boluses to pass and prevent stomach contents from refluxing
What is the Z-line?
The line where oesophageal mucosa abruptly changes to gastric mucosa
This marks the boundaries of each structure
Describe the structure and function of the pyloric sphincter
Circular muscle coat at the end of the pyloric portion of the stomach is thickened to form an anatomical sphincter
Regulates the passage of chyme into the duodenum
Label the boxes
From top left clockwise:
Diaphragm
Endothoracic fascia
Pleura
Upper phrenico-oesophageal ligament
Endoabdominal fascia
Cardiac notch
Lower phrenico-oesophageal ligament
Cardiac orifice of stomach
Z-line
Peritoneum
Label the diagram
Top to bottom:
Pyloric canal
Pyloric orifice/sphincter
Duodenum
What features of the stomach are most clearly seen when empty?
Rugae:
Longitudinal folds in the gastric mucosa
Gastric canal:
Found on the lesser curvature, a canal between gastric folds that allows saliva and small amounts of chewed food to reach the pylorus
Label this diagram, answers given in columns
Column 1:
Gastric pit
Mucous epithelium
Lymph vessel
Lamina propria
Musc. Mucosa
Submucosa
Oblique muscle
Circular muscle
Longitudinal muscle
Serosa
Column 2:
Gastric pit
Artery + Veins
Gastric gland
Myenteric plexus
Column 3:
Mucous cells
Neck
Pariteal cells
Chief cells
Smooth muscle cell
G cell
Outline how the stomach has regions that are histologically distinct from each other
Different zones carry different types of cells in their gastric pits
Cardia:
Only neck cells
Fundus and Body:
Neck cells
Parietal cells
Chief cells
Pylorus:
Neck cells
G-cells
Describe the greater omentum
Prominent, four layered peritoneal fold hanging like an apron from the greater curvature
After descending it folds back up and attaches to the anterior transverse colon and its mesentery
Describe the lesser omentum
Small, double layered peritoneal fold that connects the lesser curvature of the stomach and the proximal part of the duodenum to the liver
Also connects the stomach to the portal triad
Describe the epiploic foramen
Opening siutated posterior to the free edge of the lesser omentum (hepatoduodenal ligament)
Label the boxes
Top to botom, left to right:
Lesser omentum
Finger inserted into epiploic foramen
Greater omentum
What is the coeliac trunk?
Branch of the abdominal aorta at the level of T12
Gives rise to the splenic, left gastric and common hepatic arteries
Supplies blood to the liver, stomach, abdominal, oesophagus, spleen and the superior half of both the duodenum and the pancreas.
Label this diagram
Top left clockwise:
Left gastric artery
Oesophageal branch of left gastric
Aortic hiatus
Posterior gastric artery
Splenic artery
Short gastric arteries
Spleen
Left gastro-omental artery
Abd. Aorta
Right gastro-omental artery
Superior pancreaticoduodenal artery
Supraduodenal artery
Gastroduodenal artery
Common hepatic artery
Right gastric artery
Hepatic artery proper
Cystic artery
Coeliac trunk
Describe the blood supply to the lesser and greater curvature and the fundus and body of the stomach
Lesser curvature:
Left gastric (branch of the coeliac trunk)
Right gastric (branch of the common hepatic)
Greater curvature:
Left gastro-omental (branch of the splenic)
Right gastro-omental (branch of the gastro-duodenal, in turn a branch of the common hepatic)
Fundus and body:
Posterior/small gastric arteries (branches of the splenic)
Label this diagram
Top left anti-clockwise:
Left gastric vein
Right gastric vein
Portal vein
Pre-pyloric vein
Pancreaticoduodenal vein
Right gastro-omental vein
Splenic vein
Left gastro-omental vein
Middle gastric vein
Short gastric vein
