S4: stomach physiology & pathology

Question 1

Describe the functions of the stomach

Answer 1

Storage facility
Starts digestion of proteins
A little bit of carb and fat digestion (salivary amylase & lingual lipase)
Disinfect – innate defence (hostile to any microorganisms)

Question 2

Describe the anatomy of the stomach

Answer 2

3 parts – fundus, body & antrum
2 sphincters – lower oesophageal sphincter & pyloric sphincter
Stomach lining (simple columnar) has rugae so it can expand without increasing pressure too much

Question 3

Describe the lower oesophageal sphincter

Answer 3

Intrinsic smooth muscle & right crus of diaphragm (loops around the sphincter & acts to close it when intra-abdominal pressure increases)
Can stop reflux – acute angle of entry also helps

Question 4

Describe receptive relaxation

Answer 4

Peristalsis causes reflex relaxation of proximal stomach = RECEPTIVE RELAXATION
Fundus distends
Stomach can fill without significant rise in pressure

Question 5

Describe the muscles of the stomach

Answer 5

3 layers – oblique, circular & longitudinal
Cause forceful contractions to mix and grind contents
Thinner walled proximally and more muscular distally – can be dilated proximally & is narrowed distally

Question 6

Describe the surface of the stomach

Answer 6

Surface mucous cells – produce mucus which forms a protective layer to protect epithelium from the acidic conditions
Gastric pits – invaginations of the epithelium
-in the pits, there are gastric glands which have 3 types of cells: parietal cells, chief cells & G cells

Question 7

Describe the mechanisms that exist to protect the stomach epithelia against an acidic environment

Answer 7

Stomach is made of protein – needs to protect itself from the proteases

1) High turnover of epithelial cells – if one gets damaged, replaced quickly to keep barrier intact
2) Production of alkaline mucus layer
3) Prostaglandins – increase mucosal blood flow, which supports the mucus layer

Question 8

Describe the different states of the parietal cell

Answer 8

Resting phase – tubulovesicles (contain proton pumps, lack K+ permeability) and apical membrane (contains K+ channels) are not in contact
Stimulated phase – canaliculi cause the tubulovesicles and apical membrane to be in contact – H+ can be secreted in exchange for K+

Question 9

What stimulates acid production?

Answer 9

1) Sensory triggers – smell, taste & sight (CEPHALIC PHASE – 30% OF HCL)
2) Gastric triggers – stretch & presence of amino acids + small peptides (GASTRIC PHASE – 60% OF HCL)
3) Intestinal triggers – chyme in duodenum -> presence of partial digested proteins (INTESTINAL PHASE – 10% OF HCL)

Question 10

List the three ways a parietal cell is stimulated

Answer 10

1) Gastrin receptors
2) Histamine receptors
3) Muscarinic receptors

Question 11

Describe gastrin stimulation of parietal cells

Answer 11

Peptides in stomach lumen stimulate G cell
G cell produces gastrin
Gastrin binds to CCK receptor on parietal cell

Question 12

Describe vagal stimulation of parietal cells

Answer 12

Can stimulate G cells to produce gastrin -> binds to CCK receptor
GRP and ACh binds to receptors on G cell
Also directly binds to muscarinic receptors on parietal cells

Question 13

Describe histamine stimulation of parietal cells

Answer 13

ECL (entero-chromaffin like cell) – produces histamine which goes on to bind to H2 receptor on parietal cell
ECL has muscarinic & CCK receptor which stimulates it to produce histamine

Question 14

Describe how acid secretion is inhibited

Answer 14

Drop in pH detected by D cell
D cell produces somatostatin
Inhibits secretion of gastrin

Question 15

How is HCl produced in the parietal cell?

Answer 15

H20 and CO2 combine to produce H2CO3 (catalysed by carbonic anhydrase)
Carbonic acid then spontaneously dissociates into H+ and HCO3-
H+ transported into stomach lumen by the H+/K+/ATPase
HCO3- is transported out of the cell by the anion exchanger (Cl- comes in; this is transported into the stomach lumen via chloride channel)
H+ and Cl- combine in lumen to produce HCl
Alkaline tide – transient rise in blood pH due to bicarbonate

Question 16

Define dyspepsia

Answer 16

Complex of upper GI tract symptoms which are typically present for four or more weeks
Include upper abdominal discomfort, heartburn, acid reflux, nausea and/or vomiting

Question 17

Describe gastro-oesophageal reflex disease (GORD)

Answer 17

Reflux of stomach contents into oesophagus
Symptoms: heart burn, acidic taste (potential dental erosion), cough & asymptomatic
Risk factors: obesity, pregnancy, LOS dysfunction, hiatus hernia & delayed gastric emptying

Question 18

What is a hiatus hernia?

Answer 18

LOS herniates through diaphragm into the thorax – loss of crural muscles

Question 19

Describe complications of GORD

Answer 19

Oesophagitis
Ulceration
Haemorrhage 
Strictures (scar tissue)
Metaplastic changes

Question 20

What is Barrett’s oesophagus?

Answer 20

Reversible change of stratified squamous epithelia to columnar epithelia due to repeated exposure to gastric contents
Columnar -> increases risk of dysplasia -> adenocarcinoma

Question 21

Describe management of GORD

Answer 21

Lifestyle – weight loss, avoiding trigger foods, eat smaller meals, don’t eat then sleep, decrease alcohol and caffeine & stop smoking
Drugs – proton pump inhibitors (symptom relief & healing inflammation), H2 receptor antagonists
Surgery – fundoplication (fundus is wrapped around the lower oesophagus)

Question 22

What is gastritis?

Answer 22

Inflammation of the stomach mucosa
Symptoms: pain, nausea, vomiting, haemorrhage
Acute causes: NSAIDS, alcohol, chemotherapy, bile reflux
Chronic causes: infection with H-pylori, autoimmune

Question 23

Describe the pathological changes in acute and chronic gastritis

Answer 23

Acute 
1) Epithelial damage
2) Some epithelial hyperplasia 
3) Vasodilation 
4) Neutrophil response – infiltrate the lamina propria
Chronic
1) Lymphocyte response 
2) Glandular atrophy 
3) Fibrotic changes
4) Metaplastic changes

Question 24

Describe how an autoimmune response causes chronic gastritis

Answer 24

Antibodies to parietal cells
Lose parietal cells -> decreased acid production & decreased intrinsic factor
Symptoms – megaloblastic anaemia, neurological symptoms, anorexia & glossitis
Decreased vitamin B12 absorption (can’t be produced in the body)

Question 25

Describe H-pylori

Answer 25

Helix shape, gram negative, faeco-oral or oral-oral transmission
Microaerophilic – needs some O2 – stomach has the correct O2
Features: flagellae, chemotaxis & adhesins
Contain urease – converts urea + H20 -> CO2 + ammonia (base); produces a local environment where it is less acidic

Question 26

Describe how H-pylori causes chronic gastritis

Answer 26

Cytotoxin associated gene A – causes inflammation (increases risk of stomach cancer)
Vacuolating toxin A – toxic to stomach epithelium
Ammonia causes damage to stomach epithelium (urease reaction)
Produces mucinase (damage mucus layer), protease & lipase

Question 27

Describe H-pylori interactions in different parts of the stomach

Answer 27

Antrum – causes over-activity of G cells -> stimulates parietal cells
-too much acid produced & makes chyme leaving the stomach more acidic
Body/fundus – atrophy of the parietal cells
-precursor to dysplastic changes

Question 28

How is H-pylori diagnosed?

Answer 28

1) Urea breath test – get patients to ingest enriched C13 urea – if present, should breathe out C13 CO2
2) Stool antigen test
3) Endoscopy with biopsy

Question 29

How is H-pylori eradicated?

Answer 29

Proton pump inhibitor & 2x antibiotics
Side effects: diarrhoea & nausea
Do for 7 days – check success with urea breath test (can be increased to 14 days)

Question 30

Describe peptic ulcer disease

Answer 30

Defect in the gastric/duodenal mucosa that extends through the muscularis mucosa
Most common place: first part of duodenum & lesser curve of stomach
Gastric ulcers – 70% have H-pylori
Duodenal ulcers – 95-100% have H-pylori

Question 31

List risk factors for peptic ulcer disease

Answer 31

H-pylori
NSAIDS – decreased prostaglandin synthesis
Smoking
Massive physiological stress

Question 32

Describe the difference between acute and chronic ulcers

Answer 32

Acute – develop as part of gastritis

Chronic – occur at mucosal junctions

Question 33

Describe the morphology of PUD

Answer 33

Base of ulcer is made of necrotic & granulation tissue, when heals it is replaced by scar tissue (muscularis externa)
Can narrow the stomach lumen – pyloric stenosis (causes extensive vomiting) if near sphincter
Peritonitis (inflammation of the peritoneal cavity) can occur if ulcer extends all the way through the gut wall -> gut contents can leak out

Question 34

Describe what happens if an ulcer erodes into a blood vessel

Answer 34

Malaena – black stools
Upper GI bleed -> Haem component is oxidised by passing through the GI tract
If gastro-duodenal artery (most likely)/splenic artery (very rare) is affected – massive haemorrhage of blood & haematemesis (vomiting of blood)

Question 35

List symptoms of PUD

Answer 35

Epigastric pain – back pain following meals
Pain at night – duodenal ulcers
Resulting from bleeding – haematemesis & malaena
Early satiety
Weight loss

Question 36

Describe the management of PUD

Answer 36

No active bleeding:
1) H-pylori positive: eradicate H-pylori – promotes ulcer healing
2) H-pylori negative: stop exacerbating medications
Active bleeding:
Adrenaline is injected + cautery +/- clip application
If ulcer is perforated will need to have open surgery
After intervention, test for H-pylori (if present, eradicate)