Functions of the Stomach Flashcards
1
Q
State the functions of the stomach
A
- Receive/store food
- Disrupt food
- Continue digestion
- Disinfect
2
Q
What adaptabilities help the stomach store food
A
- Receptive relaxation:
- Vagally mediated relaxation of orad stomach
- Allows food to enter stomach without raising intra-gastric pressure too much
- Prevents reflux of stomach contents during swallow
- Rugae allow distension
3
Q
Describe the regions of the stomach
A
- Cardia at the LOS opening
- Fundus on the superior border of stomach
- Body in the middle
- Antrum near the pylorus
4
Q
Describe the epithelium of the stomach
A
- From lower oesophagus to stomach
- Abrupt transition of stratified squamous to columnar epithelium
- Columnar epithelium more suited to secretion
- Abrupt transition of stratified squamous to columnar epithelium
5
Q
Explain the actions of smooth muscle in the stomach
A
- Extra oblique layer of muscle in stomach in addition to circular and longitudinal muscle
- Help contract and grind food
- Contractions
- Mix/grind food and move contents along
- Upper stomach has sustained contractions
- Creates basal tone
- Thinner epithelium to allow more relaxation when lots of food content
- Lower stomach has thicker and more muscular walls
- Strong peristalsis mixes stomach contents
- Coordinates movements - contractions every 20 seconds
6
Q
Describe the components of gastric secretion and their cellular origins
A
- HCl - parietal cell
- Intrinsic factor - parietal cell
- Mucus/HCO3 - gastric mucous cells
- Pepsinogen - chief cell
7
Q
Describe where acid is released in the stomach
A
- H+ (acid) is released from parietal cells in the stomach
- A proton (H+) pump is located within parietal cells to release H+
- H+ requires lots of ATP
8
Q
What is the alkaline tide
A
- During digestion of food in the stomach, HCO3 produced
- HCO3 enters capillary and increases pH of blood leaving stomach
9
Q
How is acid production increased
A
- Gastrin binds to CCK receptor on parietal cells
- Histamine binds to H2 receptors
- ACh from vagus nerve bind to muscarinic receptors
10
Q
How is gastrin secretion controlled
A
- Produced by G cells located in antrum
- G cells stimulated by:
- Peptides/amino acids in stomach lumen
- Protein breakdown products stimulate more acid release
- Vagal stimulation - acetylcholine and gastrin-releasing peptide (GRP)
- Start releasing acid when see/smell food to prepare stomach
- Peptides/amino acids in stomach lumen
- Vagus nerve controls both G cells and parietal cells to allow a finely balance of acid concentration
11
Q
How is acid production inhibited
A
- Essentially an inhibition of G cells
- When food leaves stomach, pH drops
- Food acts as a buffer
- Low pH activates D cells
- D cells release somatostatin which inhibits G cells (and ECL cells)
- Stomach distension reduces
- Reduced vagal activity
12
Q
Describe the function of the stomach defences
A
- Body is made of proteins
- Stomach protects itself from digestion by secreting mucus containing dissolved HCO3
- Mucus/HCO3
- Released by surface mucus cells and neck cells in gastric glands
- Forms thick alkaline viscous layer that adheres to epithelium
- Epithelial surface kept at higher pH
- High turnover of epithelial cells
- Helps keep epithelia intact
- Prostaglandins
- Maintain mucosal blood flow
- Supplying epithelium with nutrients to help secrete mucus and HCO3
- Non-steroidal drugs inhibit prostaglandins
- Cause damage
- Maintain mucosal blood flow
13
Q
Describe the symptoms of GORD
A
- Heartburn, cough, sore throat, dysphagia (difficulty swallowing)
14
Q
Describe the causes of GORD
A
- Lower oesophageal sphincter problems
- Delayed gastric emptying (raised intra-gastric pressure)
- Hiatus hernia - herniate cardia through diaphragm into thorax
- Obesity
15
Q
Describe the consequences of GORD
A
- Oesophagitis
- Strictures
- Barrett’s oesophagus
- Metaplasia of squamous epithelium to columnar
- Increased risk of developing adenocarcinoma
- Adenocarcinoma not normally seen in oesophagus and normally squamous cell carcinoma
16
Q
Describe the treatment of GORD
A
- Lifestyle modifications - decrease weight, not sleeping flat, eating earlier before sleep
- Pharmacological
- Antacids - layer over epithelium to prevent acid secretion
- H2 antagonists - prevent histamine activating parietal cell
- Proton pump inhibitors - decrease acid production
- Surgery (rare)
17
Q
Describe causes of acute gastritis
A
- Heavy use of NSAIDS - decrease prostaglandins -> decrease blood flow -> inflammation
- Lots of alcohol
- Chemotherapy
- Bile reflux
18
Q
Describe the symptoms of acute gastritis
A
- Asymptomatic
- Or pain, nausea, vomiting
- Occasionally bleeds - can be fatal
19
Q
Describe the causes of chronic gastritis
A
- Bacterial - H-pylori infection
- Autoimmune - antibodies to gastric parietal cells
- Parietal cells cannot produce intrinsic factor
- If infected, cannot absorb B12 and can lead to pernicious anaemia
- Symptoms - symptoms of anaemia
- Glossitis - big red tongue
- Anorexia
- Neurological symptoms
20
Q
Define peptic ulcer disease
A
- Defects in gastric/duodenal mucosa
- Must extend through muscularis mucosa
21
Q
Give causes of peptic ulcer disease
A
- Stomach acid
- H-pylori
- NSAIDS
- Zollinger-Ellison disease
- Smoking - only contributes to relapse of ulcer disease
- Stress
22
Q
What are symptoms of peptic ulcer disease
A
- Epigastric pain (foregut) - sometimes back pain
- Burning/gnawing
- Follows meal times
- Acid in contact with ulcer during digestion - very serious pain 1 hour after eating
- Often at night
- Bloating
- Vomiting
- Bleeding/anaemia - if blood vessels affected
- Ulcer on the lesser curve of the stomach can erode into the left gastric artery
- Duodenal ulcer can erode into the gastro-duodenal artery
- Perforation - undigested food enters peritoneal space
- Air can irritate the phrenic nerves to the diaphragm, leading to referred pain to C3-C5
- Obstruction
- Early satiety
- Weight loss
23
Q
Describe Zollinger-Ellison disease
A
- Gastrin secreting tumour - stimulate parietal cells and therefore produce more acid
- Leads to ulceration of stomach and small intestine
24
Q
How are investigations for upper GI pathology carried out
A
- Upper GI endoscopy - biopsies (benign, malignant, H-pylori)
- Urease breath test - detect H-pylori
- Erect chest x-ray - perforation - gas in peritoneal cavity
- Blood test - anaemia
25
Q
Describe the treatment for gastric pathology
A
- Eradicate H-pylori
- Stop NSAIDS
- Endoscopy for bleeding ulcers
- Proton pump inhibitors
- Antacids
26
Q
Describe the spread and shape of H. pylori
A
- Fecal to oral
- Helix shaped/gram negative/microaerophilic
27
Q
Describe some virulence factors of H. pylori
A
- Produces urease
- Converts urea to ammonium (basic in solution)
- Increases local pH to survive acidic environment
- Converts urea to ammonium (basic in solution)
- Has flagellum
- Good motility
- Lives in mucus layer/adheres to gastric epithelia
28
Q
Describe how H. pylori causes problems
A
- Releases cytotoxins (proteases) - direct epithelial injury
- Expresses enzymes
- Urease - ammonia toxic to epithelia
- Possibly degrades mucus layer
- Promotes inflammatory response - self injury
29
Q
Describe how different parts of the stomach specialise in different roles
A
- Cardia predominantly mucus secretion
- Fundus/body mainly mucus, HCl and pepsinogen secretion
- Antrum mainly gastrin and somatostatin
30
Q
Describe how different parts of the stomach which are infected by H. pylori can have different consequences
A
- If in antrum (home of G cells) - duodenal ulceration
- If in antrum and body - asymptomatic
- Area that produces acid inflamed so decreased acid production
- If predominantly in body - can lead to cancer
31
Q
Outline the ways in which gastric acid secretion may be reduced by drugs
A
- Pharmacological intervention
- H2 blockers
- Proton pump inhibitors
- Medication can be given to coat the stomach to prevent acidic damage (antacids)
