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Gastrointestinal > Lecture 7- the stomach > Flashcards

Lecture 7- the stomach Flashcards

1
Q

Function of the stomach

A
  1. Storage facilit
  2. Start digestion
  3. Carb and fat digestion
  4. Disinfect –> innate defence acid
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2
Q

part of the stomach that is closest to the oesophagu

A

cardia

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3
Q

top of the heart

A

fundus

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4
Q

middle of the heart

A

body

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5
Q

bottom part of the stoamch

A

pylorus

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6
Q

part of stomach leading to the duodenum

A

pylorus

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7
Q

which cells line the oesophagus

A

stratified squamous

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8
Q

which cells line the stomach

A

simple columnar of the stomach

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9
Q

the Lower oesophageal sphincter

A

stops reflux into the stomach from SI

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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)
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11
Q

what also stops food coming back of

A

angle of the stomach

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12
Q

Receptive relaxation

A
  • peristalsis causes reflex relaxation of proximal stomach–> fundus distends–> creates more space
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13
Q

layers of the stomach

A
  • Oblique (outside
  • Circular
  • Longitudinal
    • Forceful contractions to breakdown food
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14
Q

…….. wall the top

……..wall at the bottom

A
  • Thinner wall at the top
  • Thicker wall at the bottom
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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
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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
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17
Q

gastric pits in the antrum…

A
  • More prevalent G cells- enteroendocrine cells
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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.
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19
Q

acid producing cells

A

parietal cells

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20
Q

parietal cells produce acid by

A

exhcnaging potssium for hydrogen via a proton pump

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21
Q

parietal cells have

A

a resting phase- dont want to produce acid all the time

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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
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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
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24
Q

Phases of digestion

A
  • Cephalic phase (30% HCL)
  • Gastric- 60%
  • Intestinal- 10%
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25
Q

what turns opn the parietal cell

A
  1. gastrin receptor
  2. histaminw receptor
  3. muscarinic receptor
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26
Q

how does the gastrin receptor turn on parietal cells (to produce HCL)

A
  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
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27
Q

how does the histamine receptor turn on parietal cells (to produce HCL)

A
  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
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28
Q

how does the muscarinic receptor turn on parietal cells (to produce HCL)

A
  1. Vagus stimulation- release Ach
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29
Q

Drop in pH triggers

A

D cells to produce somatostatin which inhibits G cells to stop producing gastrin via somatostatin receptor.

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30
Q

how is acid produced by parietal cells

A
  • 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
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31
Q

Gastric disease- dyspepsia

A

“ 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”

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32
Q

GORD stands for

A

gastric oesophageal reflux disease (GORD)

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33
Q

symptoms of GORD

A
  • Symptoms related to stomach complex reflux into oesophagus up to the larynx
    • Heart burn
    • Acidic taste – dental erosion
    • Cough
    • Sore throat
    • Asymptomatic
34
Q

Risk factors of GORD

A
  • 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
Q

3 factors which cause the oesophageal sphincter to work?

A
  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
Q

why is LOS reflux more common than pylroic sphincter reflux

A
  • 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
Q

complications of GORD

A
  • Oesophagitis- bile and acid and pepsin
  • Ulceration
  • Haemorrhage- anaemia
  • Fibrous structures
  • Barrertts oesophagus
38
Q

Barrett’s oesophagus

A

Metaplastic reversible change of stratified squamous epithelial —>columnar due to repeated exposure to gastric contents

  • Risk of dysplasia adenocarcinoma
39
Q

treatment of GORD

A
  • Weight loss
  • Avoid trigger foods
  • Eat smaller meal
  • Don’t eat then sleep
  • Reduce alcohol and caffeine
  • Stop smoking
40
Q

drugs to treat GORD

A
  • Proton pump inhibitors- symptom relief and healing inflammation
  • H2 receptor antagonists
41
Q

surgery for GORD

A

fundoplication

fundus is wrapped around the lower oesophagus to help sphincter mechanism

42
Q
A
43
Q

Gastritis

A

Inflammation of the stomach mucosa

44
Q

symptoms of gastritis

A
  • Complex symptoms
    • Pain
    • Nausea
    • Vomiting
    • Haemorrhage
    • Endoscopic appearance can be used
45
Q

acute gastritis causes

A
  • Can go on to become chronic
  • Causes
    • NSAIDs
    • Alcohol
    • Chemo
    • Bile reflux (stomach not used to- produced in SI- chemical injury)
46
Q

pathological changes associated with acute gastirtis

A
  • Epithelia damage
  • Some epithelial hyperplasia
  • Vasodilation  angry looking
  • Neutrophil response
47
Q

chronic gastirtis causes

A
  • Long lasting stimulus
  • Causes
    • H. pylori
    • Autoimmune
48
Q

pathologcal causes associated with chronic gastritis

A
  • Lymphocyte response
  • Glandular atrophy
  • Fibrotic changes
  • Metaplastic changes
49
Q

autoimmune chronic gastritis

A
  • 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
Q

in autoimmiuen chronic gastritis, antibodies stop

A

acid and intrinsic factor from being absorbed

51
Q

symptoms of autoimmune chronic gastirtis

A
  • Anaemia- megaloblastic anaemia
  • Neurological symptoms
  • Glossitis- inflamed tongue
  • Anorexia
52
Q

how much fo world pop infected by H. Pylori

A
  • Infected 50% of world pop
  • Asymptomatic in majority
  • May have some benefits
  • Implicated in gastritis
53
Q

Helicobacter pylori

A
  • helix shaped
  • gram negative
  • microareophilic (needs some O2- stomach as correct amount)
54
Q

H. pylori mode of infection

A

faecal oral route

55
Q

how does H. pylori adhere to the epithelial lining of the stomach

A
  1. Flagella (using chemotaxis to find higher pH regions)
  2. Adhesion fix to gastric epithelial- resist peristalsis
  3. Has its own cytoplasmic urease
56
Q

cytoplasmic urease and pylori

A

produced in cytoplasm of H.pylori (gram neg rod)

Ureas + H2O–> CO2 + ammonia = basic (protect against stomach acid)

*Toxic to our epithelial cells

57
Q

how does h. pylori cause damage to the stomach lining

A
  • 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
Q

Antral colonisation by H.pylori–

A

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
Q

Fundus and body colonisation by h. pylori -

A

atrophy of the parietal cells- precursor to dysplastic changes- risk of stomach cancer

60
Q

how is H. pyrlori treated

A

3 pronged approach

  1. Proton pump inhibitor
  2. x 2 antibiotics e.g. clarithromycin and metronidazole (7 days up to 14)
61
Q

diagnosis of pylori

A

urea breath test

stool antigen test

endoscopy with biopsy

62
Q
  • Urea breath test
A
  • 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
Q

Peptic ulcer disease

A

Defect in the gastric or duodenal mucosa that extends through the muscularis mucosa

64
Q
  • Symptoms of peptic ulcer disease
A
    • 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
Q

location of peptic ulcer disease

A
  • duodenum (most common)
  • gastric ulcers
66
Q

duodenal peptic ulcers

A
  • 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
Q

stomach peptic ulcers

A
  • 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
Q
  • Risk factors (interfering with stomach defences)
A
  • H pylori
  • NSAIDS decrease prostaglandin synthesis
  • Smoking  contribute to relapse
  • Massive physiologic stress (e.g. burns)
69
Q

acute peptic ulcers develop as part of

A

acute gastirtis

70
Q

chronic peptic ulcers occur

A
  • Occur at mucosal junctions e.g. where the antrum meets the body and where the antrum meets the small intestine
71
Q

Stomach defences

A
  • 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
Q

peptic ulcers can be up to

A

10cm

73
Q

base of ulcer made up of

A

necrotic tissue

74
Q

with peptic ulcers the muscularis externa replaced by

A

scar tissue- can narrow the stomach lumen- pyrloric spincter stneosis- vomiting

75
Q

risk of peptic uclers

A
  • 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
Q

Peptic ulcer can haemorrhage a vessel at the base of the ulcer very slowly

A
  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
Q

largest risk of peptic ulcers

A
  • 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
Q

Management of peptic ulcer disease

  • No active bleeding
  • H pylori positive
A
  • Eradicate H-pylori
    • Treatment
      • PPI
      • Ab
      • Ab
79
Q

Management of peptic ulcer disease

no active bleeding

  • H pylori negative
A
    • Stop exacerbating medications e.g. NSAIDS
80
Q

Management of peptic ulcer disease

Active bleeding

A
  • Endoscope- adrenaline injected and cautery +/- clip application

After intervention- test for H pylori and removed

Gastrointestinal (35 decks)

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