S5) Function and Pathology of the Stomach Flashcards
1
Q
What do epithelial cells do in the stomach?
A
Epithelial cells cover the surface and extend into pits/glands
2
Q
Identify 4 epithelial cells in the stomach
A
- Mucous cells
- Parietal cells
- Chief cells
- G cells
3
Q
Identify the muscle layers in the stomach
A
- Circular
- Longitudinal
- Oblique
(the shape of the stomach also means that food has to travel downwards)
4
Q
What is the effect of stomach muscle contractions?
A
- Mix/grind contents
- Move contents along
5
Q
What is the function of the upper stomach?
A
The upper stomach has sustained contractions (tonic) to create basal tone
slow
6
Q
The lower stomach is more muscular.
Describe its function
A
The lower stomach has strong peristalsis which mixes stomach contents
7
Q
Describe how contractions occur in the stomach
A
- Contractions are coordinated
- Contractions occur every 20 seconds
- Contraction are proximal to distal
8
Q
What is receptive relaxation?
A
Receptive relaxation is the vagally mediated relaxation of orad stomach
9
Q
What is the purpose of receptive relaxation?
A
- Allows food to enter stomach without raising intra-gastric pressure too much
- Prevents reflux of stomach contents when swallowing
- Gastric mucosal folds (rugae) allow distension
10
Q
Identify 3 functions of the acidic conditions of the stomach
A
- Helps unravel proteins
- Activates proteases: pepsinogen → pepsin
- Disinfects stomach contents
11
Q
Identify 4 substances which are secreted by the stomach
A
- HCl
- Intrinsic factor
- Mucus/HCO3-
- Pepsinogen (pepsin)
12
Q
Identify the substances secreted from the following cells:
- Parietal cell
- G cell
- Enterochromaffin like cell
A
- Parietal cell: HCl & intrinsic factor
- G cell: gastrin
- Enterochromaffin like cell (ECL): histamine
13
Q
Identify the substances secreted from the following cells:
- Chief cell
- D cells
- Mucous cells
A
- Chief cell: pepsinogen
- D cells: somatostatin
- Mucous cells: mucus
14
Q
Identify the substances secreted from the following regions in the stomach:
- Cardia
- Fundus/body
- Pylorus
A
- Cardia: predominantly mucus secretion
- Fundus/body: mucus, HCL, pepsinogen
- Pylorus: gastrin, somatostatin
15
Q
Identify the 3 substances which stimulate HCl production and state their origins
A
- Gastrin from G cell
- Histamine from ECL cells
- Acetylcholine from vagus nerve
16
Q
Where are G cells located?
A
G cells located in antrum
17
Q
Identify the 2 factors which stimulate Gastrin secretion
A
- Peptides/AA in stomach lumen
- Vagal stimulation: (parasympathetic)
I. Acetylcholine
II. Gastrin-releasing peptide (GRP)
gastrin binds to CCK receptors
18
Q
When food leaves the stomach, the pH drops.
How can HCl production be inhibted?
A
- Low pH stimulates D cells which release somatostatin
- Somatostatin inhibits G cells and ECL cells
- Stomach distension reduces due to reduced vagal activity
19
Q
Identify the 3 phases of digestion
A
- Cephalic
- Gastric
- Intestinal
20
Q
How much HCl is produced in the cephalic phase?
A
30% of total HCl
21
Q
Outline the parasympathetic stimuli in the cephalic phase of digestion
A
- Smelling, tasting, chewing, swallowing (sensory triggers)
- Direct stimulation of parietal cells by vagus nerve
- Vagus nerve releases GRP which stimulates of G cells
22
Q
How much HCl is produced in the gastric phase of digestion?
A
60% of total HCl
23
Q
State 4 events which occur in the gastric phase of digestion
A
- Stomach distension and stretch stimulates vagus nerve
- Vagus nerve stimulates parietal cells and G cells
- Amino acids and small peptides stimulates G cells
- Presence of food acts removes inhibition on Gastrin production (buffer) and the pH increases slightly
24
Q
What is the role of the enteric nervous system in the gastric phase of digestion?
A
ENS and gastrin causes strong smooth muscle contractions
25
How much HCl is produced in the intestinal phase of digestion?
10% of total HCl production
26
State the 4 events occurring in the intestinal phase of digestion
- Chyme **stimulates gastrin secretion** due to the detection of partially digested proteins by duodenum
- G cells are then inhibited
- **Enterogastric reflex** is activated by lipids which reduces **vagal stimulation**
- Chyme then stimulates **CCK** and **secretin**
27
Which substances are released to protect the stomach lining?
- Mucus
- HCO3-
28
Where are mucus and hydrogen carbonate secreted from in the stomach?
- Surface mucus cells
- Neck cells in gastric glands
29
What are the effects of mucus and hydrogen carbonate secretion in the stomach?
- Thick alkaline viscous layer is formed which adheres to epithelium
- Epithelial surface kept at higher pH
30
Apart from mucus/HCO3-, identify and describe 2 other stomach defences
- **High turnover of epithelial cells** to keep epithelia intact
- **Prostaglandins** to maintain mucosal blood flow and supply epithelium with nutrients
31
Identify 3 substances that breach the stomach defences and state their effects
- **Alcohol** – dissolves mucus layer
- **Helicobacter pylori** – causes chronic active gastritis
- **NSAIDS** – inhibits prostaglandins
32
Up to 40% of adults suffer from dyspepsia per year.
What is dyspepsia?
**Dyspepsia** is pain/discomfort in the upper abdomen
33
Identify 6 common gastric disorders
- Gastro-oesophageal reflux disease (GORD)
- Gastritis
- Peptic ulcer disease
- Zollinger-Ellison disease
- Stress ulcers
- Stomach cancer
34
What is GORD?
**Gastro-oesophageal reflux disease** (GORD) is a digestive disorder that affects the lower oesophageal sphincter and causes the reflux of stomach acid/contents into the oesophagus
35
Identify 4 symptoms of GORD
- Heartburn
- Cough
- Sore throat
- Dysphagia
36
Identify 4 causes of GORD
- LOS problems
- Delayed gastric emptying (raised intra-gastric pressure)
- Hiatus hernia
- Obesity
37
Identify 3 compound problems which can arise from GORD?
- Oesophagitis → lots of bleeding
- Strictures → hard to swallow
- Barrett’s oesophagus (metaplasia)
38
Identify 3 types of treatment for GORD
- Lifestyle modifications: weight loss, smaller meals, don't smoke
- Pharmacological
- Surgery (rare) fundoplication → wrap funds around spinster and lowers oesophagus below diaphragm
39
Identify 3 types of pharmacological treatments for GORD
- Antacids
- H2 antagonists
- Proton pump inhibitors ( reduces symptoms and heals inflammation)
40
What is Barrett's Oesophagus?
- **Barrett’s oesophagus** is the metaplasia of squamous epithelium to columnar
- It increases the risk of developing **adenocarcinoma** (30-40x) metaplasia can turn into dysplasia where there is no turning back
41
What is gastritis?
**Gastritis** is a condition involving the inflammation of the stomach lining
42
What are the 2 types of gastritis which can occur in the body?
- Acute (can then lead to chronic)
- Chronic
43
Acute gastritis is an acute mucosal inflammatory process.
Identify 4 of its causes
- Heavy use of NSAIDS
- Lots of alcohol
- Chemotherapy
- Bile reflux
44
Identify the possible symptoms which may arise from acute gastritis
- Either: asymptomatic
- Or: pain, nausea, vomiting and occasional bleeding
45
What are the 2 types of chronic gastritis which can occur in the body?
- Autoimmune
- Bacterial
46
Compare and contrast the causes of chronic autoimmune and bacterial gastritis
- **Bacterial Gastritis** – caused by H. pylori infection (commonly)
- **Autoimmune** **Gastritis** – caused by antibodies to gastric parietal cells
47
Identify a complication of chronic autoimmune gastritis
Autoimmune gastritis can lead to **pernicious anaemia**
1. antibodies attack parietal cells
2. reduced acid production and intrinsic factor
3. less intrinsic factor → reduced absorption of B 12
4. less absorbed in the ilium
48
Identify the possible symptoms which may arise from chronic bacterial gastritis
- Either: asymptomatic
- Or: pain, nausea, vomiting and occasional bleeding
49
In chronic bacterial gastritis, symptoms may develop due to complications.
Identify 3 of its complications
- Peptic ulcers
- Adenocarcinoma
- MALT lymphoma
50
Identify the symptoms of chronic autoimmune gastritis
- Symptoms of anaemia
- Glossitis (swelling of tongue)
- Anorexia (hard to eat)
- Neurological symptoms
51
What is peptic ulcer disease?
**Peptic ulcer disease** is a condition which occurs when ulcers form and extend into the muscularis mucosae of the stomach due to defects in the gastric/duodenal mucosa
52
Identify 2 common locations of peptic ulcers
- Most common in first part of duodenum
- Commonly affects lesser curve of stomach
53
Peptic ulcer disease is caused by mucosal injury.
Identify 3 factors which may cause/contribute to this injury
- Stomach acid
- H. pylori
- NSAIDS
54
A major symptom of peptic ulcer disease is epigastric pain.
Describe the features of this pain
- Burning/gnawing
- Follows meal times
- Often at night (especially DU)
55
Identify 3 serious symptoms of peptic ulcer disease
- Bleeding/anaemia
- Satiety (early)
- Weight loss → early satiety as stomach can't expand due to scar tissue
56
What is Zollinger-Ellison syndrome?
**Zollinger-Ellison syndrome** is a condition when 1/more gastrin-secreting tumors (gastrinoma) form in your pancreas and duodenum
57
What is stomach cancer?
**Stomach cancer** is a condition which involves tumour formation in the stomach lining
58
Identify 4 different means of diagnosing gastric pathology
- Upper GI endoscopy (biopsies/H-pylori)
- Urease breath test
- Erect chest X-ray (perforation)
- Blood test (anaemia)
59
Identify 3 ways of treating gastric pathologies
- Eradicate H-pylori (PPI+ Clarithromycin + Amoxicillin)
- Stop NSAIDS
- PPIs
60
Identify 2 pharmacological interventions for gastritis and provide examples for each
- H2 blockers *e.g. cimetidine, ranitidine*
- Proton pump inhibitors *e.g. omeprazole*
61
Describe the structure, function and location of Helicobacter pylori
- **Structure**: helix shaped, gram negative, flagellum
- **Function**: produces urease, converts urea to ammonium, increases local pH
- **Location**: mucus layer/adheres to gastric epithelia
62
How does H.pylori spread?
Oral to oral/faecal to oral
63
Identify 3 of H.pylori's destructive functions
- Releases enzymes (urease) causing direct epithelial injury
- Degrades mucus layer
- Promotes inflammatory response (self injury)
64
State how the symptoms of H.pylori vary according to location
- **Antrum**: duodenal ulceration
- **Antrum and body**: asymptomatic
- **Body**: leads to cancer
65
Identify 5 causes of stress ulcerations
- Severe burns
- Raised intracranial pressure
- Sepsis
- Severe trauma
- Multiple organ failure
66
what are the different types of cells in the stomach
* stratified squamous lines the oesophagus
* simple columnar lines the cardia
67
what is the role of the right crus of the diaphragm
it is around the lower oesophageal sphincter and it closes around it when pressure starts to increase in stomach
67
what is the role of the right crus of the diaphragm
it is around the lower oesophageal sphincter and it closes around it when pressure starts to increase in stomach
68
what cells do gastric glands contain
* parietal cells (acid)
* chief cell (inactive form of pepsin - pepsinogen)
* enteroendocrine (G cells to release gastrin)
69
how does acid secretion work
* parietal cells use H/K proton pumps and exchange K for H
70
parietal cells in their resting and active states
* RESTING: apical membrane contains K and tubovesicles contain H, they are not in contact
* STIMULATED: when stimulated the tubercles move up the K and H are now in contact
71
how does histamine work to secrete acid
* ECL cells (enters-chromaffin cells) secrete histamine
* ECL can be stimulated by either vagus or Ach
* then it secretes histamine
* promotes acid secretion
72
how is HCL actually produced in the parietal cell
1. H20 + C02 → **H2co3** (carbonic acid) in the cell
2. H2co3 → Hco3- + H+ via **carbonic anhydrase**
3. **Hco3- exits cell** into the Venous blood (alkaline) via Hco3/Cl transporter
4. H passes into lumen of stomach through **H/K atpase**
5. **Cl enters the cell** as Hco3- exits into blood
6. cl moves out of the cell into lumen of stomach
7. **H + Cl → HCL**
73
what are some pathological changes in gastritis
1. epithelial damage
2. hyperplasia
3. vasodilation
4. neutrophil and lymphocyte response
5. glandular atrophy
6. fibrotic changes
74
features of H pylori which make it easy to attack the stomach
1. helix shape, gram negative, flagella and chemotaxis
2. needs some 02 stomach has the perfect amount
3. has adhesions that fix to the stomach epithelium and resist peristalsis
4. produces ammonia to change stomach pH and adapt via urease (ammonia leads to cell damage)
75
which 3 things does H pylori secrete to damage the stomach?
1. CagA → causes inflammation and increases risk factor for stomach cancer
2. VacA → toxic and increases paracellular permeability
3. mucinase, protease and lipases that break down mucus and stomach wall epithelia
76
how can H pylori spread to the duodenum?
1. stimulate G cells in the antrum
2. more parietal cells release more acid
3. chyme more acidic
4. damage cells of duodenum
5. changes to gastric cells and so colonisation of H pylori
6. can cause ulcers
77
what happens if H pylori mainly colonises in the body of the stomach
1. atrophy of parietal cells
2. increase of cancer risk
78
how to diagnose if someone is infected with H pylori
* use a urease breath test and detect amount of c13 someone exhales.
* if its higher than usual they are infected with H pylori
79
treatment of H pylori
proton pump inhibitor and antibiotics for 7 days
80
difference between acute and chronic ulcers
acute: develop as part of acute gastritis
chronic: occur at mucosal junctions
81
what are some differences between gastric and duodenal chyme
Composition: Gastric chyme is acidic and contains large food particles that have been broken down by mechanical and chemical digestion in the stomach. Duodenal chyme, on the other hand, is neutralized by bicarbonate secreted by the pancreas and contains smaller food particles that have been further broken down by enzymes.
pH: Gastric chyme has a pH of around 2-3 due to the presence of hydrochloric acid secreted by the stomach, while duodenal chyme has a pH of around 7-8 due to the neutralizing effect of bicarbonate.
Digestive enzymes: Gastric chyme contains pepsin, an enzyme that breaks down proteins, while duodenal chyme contains pancreatic enzymes such as amylase, lipase, and proteases that break down carbohydrates, fats, and proteins, respectively.
Hormonal regulation: The release of gastric chyme into the duodenum stimulates the release of hormones such as secretin and cholecystokinin (CCK) that regulate the secretion of digestive enzymes from the pancreas and gallbladder, respectively.
82
anatomy of peptic ulcer disease
scar tissue can be laid down and lead into peritonitis (inflammation of peritoneal cavity)
83
erosion of ulcers into blood vessels
1. ulcers can erode into the gastro-duodenal artery
2. this lies behind the duodenum
3. if so you get an upper GI bleed
4. malaena is present due to digestion of blood
84
how to treat peptic ulcer disease
1. if H pylori is present, eradicate
2. if its not, stop use of meds like NSAIDS
