Lecture 7- the stomach Flashcards
1
Q
Function of the stomach
A
- Storage facilit
- Start digestion
- Carb and fat digestion
- Disinfect –> innate defence acid
2
Q
part of the stomach that is closest to the oesophagu
A
cardia
3
Q
top of the heart
A
fundus
4
Q
middle of the heart
A
body
5
Q
bottom part of the stoamch
A
pylorus
6
Q
part of stomach leading to the duodenum
A
pylorus
7
Q
which cells line the oesophagus
A
stratified squamous
8
Q
which cells line the stomach
A
simple columnar of the stomach
9
Q
the Lower oesophageal sphincter
A
stops reflux into the stomach from SI
10
Q
how does the lower oesophageal sphincter stop reflux
A
- Smooth muscle- intrinsic part of the lower oesophageal sphincter
- Muscles of the diaphragm also help stop reflux (extrinsic)
11
Q
what also stops food coming back of
A
angle of the stomach
12
Q
Receptive relaxation
A
- peristalsis causes reflex relaxation of proximal stomach–> fundus distends–> creates more space
13
Q
layers of the stomach
A
- Oblique (outside
- Circular
- Longitudinal
- Forceful contractions to breakdown food
14
Q
…….. wall the top
……..wall at the bottom
A
- Thinner wall at the top
- Thicker wall at the bottom
15
Q
Epithelial surface of the stomach is lined with
A
surface mucus cells- produce mucus which protects the acidic lumen of the stomach.
- Numerous gastric pits lead onto gastric glands which contains cells of the stomach that produce acid (parietal cells) etc
16
Q
gastric pits in the body…
A
- Acid producing cells: parietal cells
- Chief cells- pepsinogen (inactive form of pepsin- protease)
- Pepsinogen –> pepsin in low pH
17
Q
gastric pits in the antrum…
A
- More prevalent G cells- enteroendocrine cells
18
Q
Stomach protective mechanism
A
- Rich blood supply and prostaglandins increase blood flow (higher HCO3) support mucus layer–> generally protective.
- epithelial cells are replaced regularly to protect the stomach.
19
Q
acid producing cells
A
parietal cells
20
Q
parietal cells produce acid by
A
exhcnaging potssium for hydrogen via a proton pump
21
Q
parietal cells have
A
a resting phase- dont want to produce acid all the time
22
Q
how is the resting phase (no acid produced) achieved
A
- Tubulovesicles (lack potassium permeability) with proton pump are not on the apical membrane in the resting phase
- Apical membrane has K+ channels
- Need to get tubulovesicles closer to the apical membrane to release HCL
- Once stimulated the tubulovesicles come together around the canaliculi
- Proton pumps and potassium channels brought close together
23
Q
What stimulates the parietal cells to produce acid?
- *
A
- Sensory triggers
- Sight
- Smell
- Taste
- Gastric triggers
- Stretch
- Presence of amino acids and small peptides
- Food acts as a buffer increasing pH
- Intestinal triggers
- Chyme in duodenum–> presence of partially digested proteins
24
Q
Phases of digestion
A
- Cephalic phase (30% HCL)
- Gastric- 60%
- Intestinal- 10%
25
what turns opn the parietal cell
1. gastrin receptor
2. histaminw receptor
3. muscarinic receptor
26
how does the gastrin receptor turn on parietal cells (to produce HCL)
1. G cell Stimulated by peptides and amino acids and vagus stimulation (ACh)
2. Produce gastrin which goes into the blood stream
3. Binds to CCK receptor
4. produces acid
27
how does the histamine receptor turn on parietal cells (to produce HCL)
1. Entero-chromaffin cells produce histamine
2. Stimulated by muscarinic receptors- ACh from vagus stimulation. Also has CCK receptor so also stimulated by gastrin
3. Which bind to HCL receptor on parietal cells
28
how does the muscarinic receptor turn on parietal cells (to produce HCL)
1. Vagus stimulation- release Ach
29
Drop in pH triggers
D cells to produce somatostatin which inhibits G cells to stop producing gastrin via somatostatin receptor.
30
how is acid produced by parietal cells
* Apical membrane has H+/K ATPase pump, K+ and Cl- pumps
* On the basal membranes HCO3-/Cl- antiport
1. Carbonic anhydrase produces H2CO3 from water and carbon dioxide
2. This dissociates to form HCO3- and H+
3. H+ is pumped out of the cell on the apical membrane in exchange for potassium which comes into the cell
4. Potassium conc of the lumen is replenished by the K+ transporter
5. The chloride channel allows Cl- to move out of the cell into the lumen and combine with H+ HCL
6. Meanwhile the Cl- conc of the cell is maintained by the HCO3-/Cl- antiport on the basal membrane
7. Influx of HCO3- into bloodstream= **ALKALINE TIDE**
31
**Gastric disease- dyspepsia**
**“** *a complex of upper GI tract symptoms which are typically present for four or more weeks, inc upper abdominal discomfort, heartburn, acid reflux, nausea and vomiting”*
32
GORD stands for
gastric oesophageal reflux disease (GORD)
33
symptoms of GORD
* Symptoms related to stomach complex reflux into oesophagus up to the larynx
* Heart burn
* Acidic taste – dental erosion
* Cough
* Sore throat
* Asymptomatic
34
Risk factors of GORD
* Increase intraabdominal pressure
* Obesity
* Pregnancy
* LOS dysfunction
* Hiatus hernia
* Lower oesophageal sphincter herniates through the abdomen and ends up in the thorax
* Delayed gastric emptying
35
3 factors which cause the oesophageal sphincter to work?
1. Muscular element of the LOS usually contracted- only relaxes when food comes down **INTRINSIC**
2. Muscular element of the diaphragm (CRUCRAL MUSCLES)- contracts sphincter- pinches it close when pressure in stomach increase **(EXTRINSIC)**
3. Angle the oesophagus joints the stomach
36
why is LOS reflux more common than pylroic sphincter reflux
* No where near as effective a sphincter as the pyloric (more muscular) sphincter at the distal end of the stomach – why LOS reflux is common
37
complications of GORD
* Oesophagitis- bile and acid and pepsin
* Ulceration
* Haemorrhage- anaemia
* Fibrous structures
* **Barrertts oesophagus**
38
**Barrett’s oesophagus**
Metaplastic reversible change of stratified squamous epithelial ---\>columnar due to repeated exposure to gastric contents
* Risk of dysplasia adenocarcinoma
39
treatment of GORD
* Weight loss
* Avoid trigger foods
* Eat smaller meal
* Don’t eat then sleep
* Reduce alcohol and caffeine
* Stop smoking
40
drugs to treat GORD
* Proton pump inhibitors- symptom relief and healing inflammation
* H2 receptor antagonists
41
surgery for GORD
fundoplication
fundus is wrapped around the lower oesophagus to help sphincter mechanism
42
43
**Gastritis**
Inflammation of the stomach mucosa
44
symptoms of gastritis
* Complex symptoms
* Pain
* Nausea
* Vomiting
* Haemorrhage
* Endoscopic appearance can be used
45
acute gastritis causes
* Can go on to become chronic
* **Causes**
* NSAIDs
* Alcohol
* Chemo
* Bile reflux (stomach not used to- produced in SI- chemical injury)
46
pathological changes associated with acute gastirtis
* Epithelia damage
* Some epithelial hyperplasia
* Vasodilation angry looking
* Neutrophil response
47
chronic gastirtis causes
* Long lasting stimulus
* Causes
* H. pylori
* Autoimmune
48
pathologcal causes associated with chronic gastritis
* Lymphocyte response
* Glandular atrophy
* Fibrotic changes
* Metaplastic changes
49
autoimmune chronic gastritis
* Antibodies against parietal cells
* Parietal cells (mainly in body of the stomach- atrophy) produce
* Acid
* Intrinsic factor production (essential for Vitamin B12 absorption in illeum)
50
in autoimmiuen chronic gastritis, antibodies stop
acid and intrinsic factor from being absorbed
51
symptoms of autoimmune chronic gastirtis
* Anaemia- megaloblastic anaemia
* Neurological symptoms
* Glossitis- inflamed tongue
* Anorexia
52
how much fo world pop infected by H. Pylori
* Infected 50% of world pop
* Asymptomatic in majority
* May have some benefits
* Implicated in gastritis
53
Helicobacter pylori
- helix shaped
- gram negative
- microareophilic (needs some O2- stomach as correct amount)
54
H. pylori mode of infection
faecal oral route
55
how does H. pylori adhere to the epithelial lining of the stomach
1. Flagella (using chemotaxis to find higher pH regions)
2. Adhesion fix to gastric epithelial- resist peristalsis
3. Has its own cytoplasmic urease
56
cytoplasmic urease and pylori
produced in cytoplasm of H.pylori (gram neg rod)
Ureas + H2O--\> CO2 + ammonia = **basic** (protect against stomach acid)
\*Toxic to our epithelial cells
57
how does h. pylori cause damage to the stomach lining
* **CagA** gene injected into stomach lining = inflammation- increased risk of stomach cancer
* **VacA** secretion- toxic
* Also secretes- **mucinase, protease and lipase**= damage mucus layer of stomach
OVERALL DAMAGE TO MUCUS LAYERS OF STOMACH
58
**Antral colonisation by H.pylori–**
over activity of G cells- stimulates parietal cells--\> too much acid produced--\> makes chyme more acidic damaging duodenum (more gastric like duodenum- can be colonised by H pylori- duodenal ulcers)
59
**Fundus and body colonisation by h. pylori -**
atrophy of the parietal cells- precursor to dysplastic changes- risk of stomach cancer
60
how is H. pyrlori treated
3 pronged approach
1. Proton pump inhibitor
2. x 2 antibiotics e.g. clarithromycin and metronidazole (7 days up to 14)
61
diagnosis of pylori
urea breath test
stool antigen test
endoscopy with biopsy
62
* Urea breath test
* Gastric urea= C12 isotopes (99%) and C13 isotopes= 1%
* Pts ingest urea with enriched C13
* H. pyrloi should convert this to ammonia and CO2
* Can detect C13 in exhaled CO2
63
**Peptic ulcer disease**
*Defect in the gastric or duodenal mucosa that extends through the **muscularis mucosa***
64
* **Symptoms of peptic ulcer disease**
* * Epigastric pain--\> back pain (burning pain) following meals
* Pain at night
* Duodenal
* Resulting from bleeding: haematemesis and melaena--\> anaemia
* Early satiety and weight loss
65
location of peptic ulcer disease
- duodenum (most common)
- gastric ulcers
66
duodenal peptic ulcers
* Most common= duodenum x3 more common than gastric ulcers
* RF
* Increase up to 35 yrs
* Blood group O
* Normal/ high acid levels
* **H. pylori- 100% of all stomach ulcers**
67
stomach peptic ulcers
* Affecting the **lesser curve or the antrum**
* Risk factors
* Age
* Social class
* Blood group A
* Normal/ low acid levels
* **H. pylori- 70% of all stomach ulcers**
68
* Risk factors (interfering with stomach defences)
* H pylori
* NSAIDS decrease prostaglandin synthesis
* Smoking contribute to relapse
* Massive physiologic stress (e.g. burns)
69
acute peptic ulcers develop as part of
acute gastirtis
70
chronic peptic ulcers occur
* Occur at mucosal junctions e.g. where the antrum meets the body and where the antrum meets the small intestine
71
**Stomach defences**
* Mucus layer- surface mucus cells
* HCO3- surface mucus cells – alkaline layer
* Mucosal blood flow needed for the mucosal layer to work well to remove acid etc
* Prostaglandins stimulated mucosal blood flow- NSAIDs work against them
* Epithelial renewal
72
peptic ulcers can be up to
10cm
73
base of ulcer made up of
necrotic tissue
74
with peptic ulcers the muscularis externa replaced by
scar tissue- can narrow the stomach lumen- pyrloric spincter stneosis- vomiting
75
risk of peptic uclers
* Can go through wall of the gut- perforation stomach content leaks out into the peritoneal cavity= peritonitis
* Can also ulcerate into the liver or pancreas
* Can haemorrhage a vessel at the base of the ulcer very slowly
76
Peptic ulcer can haemorrhage a vessel at the base of the ulcer very slowly
1. Bleed into gut- **melaena** upper GI bleed
2. Travels through GI tract
3. Haem component oxidised by passing through GI tract
4. Stool becomes black- melaena
77
largest risk of peptic ulcers
* Extensive dramatic haemorrhage
* - e.g. duodenal ulcer- if you erode posteriorly there is an artery called the gastroduodenal artery or the splenic artery (very rare)= stomach and duodenum fills with blood- haematemesis – vomiting blood
78
**Management of peptic ulcer disease**
* **No active bleeding**
* **H pylori positive**
* Eradicate H-pylori
* Treatment
* PPI
* Ab
* Ab
79
**Management of peptic ulcer disease**
**no active bleeding**
* **H pylori negative**
* * Stop exacerbating medications e.g. NSAIDS
80
**Management of peptic ulcer disease**
**Active bleeding**
* **Endoscope- adrenaline injected and cautery +/- clip application**
## Footnote
**After intervention- test for H pylori and removed**
