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Session 4 Flashcards

1
Q

2 important families of hormones in GI tract

A

Gastrin family- gastrin and cholecystokinin

Secretin family- secretin and gastric inhibitory polypeptide

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2
Q

The stomach has an impressive ability to distend in part due to

A

Rugae which are temporary folds in mucosa of stomach

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3
Q

What does the stomach have that enables it to mix and grind contents

A

3 layers of muscle

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4
Q

Stomach acid helps to

A

Unravel proteins creating a larger surface area for enzymes to act on and activates proteases in the stomach lumen

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5
Q

The mucosal surface of the stomach is comprised of

A

Gastric pits and gastric glands (parietal cells, chief cells and enteroendocrine cells)

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6
Q

Parietal cells are responsible for and stimulated by

A

Acid production in stomach

Gastrin, histamine and ACh (Acting through CCK, H2 and Mcr receptors on parietal cell)

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7
Q

Acid production increases when

A

Amino acids/peptides are detected and when the stomach is distended

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8
Q

Acid production is reduced when

A

Stomach distension reduces and a low pH is detected

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9
Q

3 phases of digestion

A

Cephalic, gastric and intestinal

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10
Q

The stomach defends itself from its acidic environment by

A

Producing a thick layer of alkaline mucus

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11
Q

Functions of the stomach

A

Storage facility
Start digestion of protein
Little bit of carb and fat digestion (salivary amylase and lingual lipase)
Disinfect = innate defence

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12
Q

Cell change when stomach starts

A

Stratified squamous before, becomes simple columnar

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13
Q

What is the opening of the stomach called

A

Cardia

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14
Q

3 divisions of stomach

A

Fundus, body and antrum

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15
Q

What is at the end of the antrum

A

Pyloric sphincter (control chyme entering duodenum)

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16
Q

What is found in the opening to the stomach

A

Lower oesophageal sphincter- made of intrinsic smooth muscle and right crus of diaphragm

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17
Q

explain the concept of receptive relaxation

A

Peristalsis causes reflex relaxation of proximal stomach

Receptive relaxation causes fundus to distend

Stomach can fill without significant rise in pressure

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18
Q

Muscle layers of stomach

A

Oblique
Circular
Longitudinal

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19
Q

Which part of stomach is more muscular

A

Posterior layer

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20
Q

Structure of gastric pit and gastric gland

A
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21
Q

Roles of parietal, chief and G cells

A
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22
Q

Protective mechanisms against stomach acid

A

Cells replaced regularly

HCO3 pH neutral layer

Prostaglandins

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23
Q

What do prostaglandins do

A

Increase mucosal blood flow
Support mucous layer
Generally protective

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24
Q

How is acid secretion by parietal cells controlled

A

H+ K+ proton pump

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25
Apical membrane contains
K+ channels
26
Tubulovesicles lack
K+ permeability
27
What happens when parietal cells go from resting to active state
Stimulated phase- canaliculi and microvilli
28
Sensory triggers for acid production
Smell, sight, taste Cephalic 30% of HCl
29
gastric triggers for stomach acid production
Stretch, presence of amino acids and small peptides Gastric 60% of HCl
30
What are the intestinal triggers for acid production
Chyme in duodenum Presence of partially digested proteins Intestinal 10% of HCl
31
How do gastrin receptors on parietal cells work
Peptides in stomach lumen are sensed by G cell, gastrin is produced (uses CCK receptor)
32
How do muscarinic receptors stimulate parietal cell
Vagal stimulation using Mcr ACh detected due to sensory triggers, GRP detected due to stretch
33
How does histamine stimulate parietal cells
Entero-chromaffin like cell ECL releases histamine
34
How is acid secretion in lumen inhibited
More HCL causes lower pH which stimulates D cell to produce somatostatin
35
How is HCL produced in the parietal cell
Carbonic anhydrase, H/KAtpase, K+ and Cl- transporters, Alkaline tide
36
What is dyspepsia
Complex of upper gastro intestinal tract
37
What is GORD
Symptoms relating to reflux of stomach contents into pharynx or oesophagus- burning chest pain, acidic taste in mouth, cough, sore throat, asymptomatic
38
Risk factors for GORD
Intra abdominal pressure Obesity Pregnancy LOS dysfunction Hiatus hernia Delayed gastric emptying
39
LOS important crus
Right crus
40
What can be refluxed
Stomach acid, Bile and pepsin (protease)- little protection in oesophagus
41
Complications of GORD
Oesophagus, ulceration, Hammorrhage, Strictures, Metaplastic changes e.g. Barett’s oesophagus
42
Barrett’s oesophagus explained
Reversible change of stratified squamous epithelia to columnar (due to repeated exposure to gastric contents) Increased risk of dysplasia, adenocarcinoma
43
usually stratified squamous epithelium could change to which form of cancer
Squamous cell carcinoma
44
Lifestyle treatments for GORD
Weight loss Avoid trigger foods Eat smaller meals Don’t eat then sleep Avoid alcohol and caffeine Stop smoking
45
Medical treatments for GORD
Drug- proton pump inhibitors give symptom relief and healing of inflammation H2 receptor antagonists Surgery- fundoplication (fundus of stomach wrapped around lower oesophagus to help with sphincter mechanism)
46
What is gastritis
Inflammation of the stomach mucosa
47
Symptom complex in gastritis
Pain, nausea, vomiting , haemorrhage
48
Acute causes of gastritis
NSAIDS Too much alcohol Chemotherapy Bile reflux
49
Chronic causes of gastritis
Infection with H pylori Autoimmune
50
Pathological changes in gastritis
Epithelial damage Epithelial hyperplasia Vasodilation (angry looking) Neutrophil response Lymphocyte response Glandular atrophy Fibrotic changes in lamina propria Metaplastic changes
51
Features of autoimmune causes of gastritis
Antibodies against our parietal cells (which produce intrinsic factor) Atrophy of parietal cells and loss of intrinsic factor
52
What is intrinsic factor for
Needed for Absorption of vitamin B 12 in Ileum
53
Symptoms of lack of intrinsic factor due to autoimmune antibodies to parietal cells
Megaloblastic anaemia Anorexia (no hunger) Neurological symptoms Glossitis (inflammation of tongue)
54
Helicobacter key facts
Infected around half of the population Asymptomatic in majority May have some benefits
55
Helicobacter bacteria features
Helix shape, gram negative, micro aero Philic, needs some oxygen, stomach has correct oxygen Transmitted by faeco-oral route into GI tract, or oral-oral route
56
Adaptations of Helicobacter
Can navigate and adhere to mucosa epithelia lining due to flagella and chemotaxis (find areas of lower acidity). Adhesions so resits peristalsis Has own cytoplasmic urease- can convert urea and water into carbon dioxide and ammonia (basic). Can resist acidic environment
57
Problem with Helicobacter
Ammonia causes cell damage CagA expresses protein which causes huge inflammatory response due to interleukin 8, implicated in cancer VacA is a secreted protein which increases paracellular permeability and is toxic Can secrete mucinases, proteases, lipases (damage mucus layer)
58
Antral colonisation of Helicobacter
Where mostly G cells located Overactivity of G cells - produce more gastrin so parietal cells produce more acid and increase in number Too much acid produced, chyme more acidic, damage to duodenum Potential conversion of duodenal epithelial cells to more gastric like epithelia. Helicobacter can then colonise duodenum and cause ulcers and further problems
59
Fundus colonisation of Helicobacter
Atrophy of parietal cells rather than over activity Precursor to dysplastic changes- increases risk of cancer
60
generally speaking if Helicobacter colonises antrum and body patients are
Asymptomatic
61
Diagnosis of H pylori
Has its own urease- Urea breath test, stool antigen test, endoscopy with biopsy
62
Explain urea breath test
Normal gastric urea contains 99% C12 and 1% C13 Can detect C13 level after being given urea enriched with C13 If C13 is higher than normal, there are h pylori present
63
Eradication of H pylori
Proton pump inhibitor, 2x antibiotics (e.g. clarithromycin and metronidazole) Side effects include diarrhoea and nausea in 5% of people 7 days usually, can double to 14 Can check if successful eradication with urea breath test
64
What is peptic ulcer disease
Defect in gastric or duodenal mucosa that extends through the muscularis mucosa
65
What must an ulceration do to qualify as a peptic ulcer
Must extend through muscularis mucosa
66
Most common place to find peptic ulcer
Duodenum not stomach- when in stomach usually in lesser curve and antrum
67
Gastric and duodenal ulcer incidence
1 gastric for every 3 duodenal Gastric increases with age, duodenal increases up to 35 Gastric more lower class gastric more common in blood group A and duodenal more common in O Acid levels normal or low in gastric ulcers (more to do with barrier defect), duodenal ulcers can cause normal or high levels (due to chyme being more acidic and overwhelming ability to neutralise) H pylori responsible for 70% gastric ulcers and 95-100% duodenal
68
Why does H pylori cause duodenal ulcers
H pylori in antrum of stomach where there are G cells Increased gastrin, proliferation of parietal cells, increased acid, increased chyme
69
Stomach defences
Mucous layer secreted by surface mucous cells (which have bicarbonate secreted into them) = alkaline layer Mucosal blood flow for repair and removal of acid Prostaglandins = stimulate blood flow e.g. reduced in NSAIDS Epithelial renewal
70
Risk factors for peptic ulcer disease
H pylori NSAIDS Smoking can cause relapse Massive physiological stress e.g. burns
71
Classification of ulcers
Acute - due to gastritis Chronic- occur at mucosal junctions
72
Morphology of peptic ulcers
Most are less than 2 cm in diameter Base is necrotic tissue, granulation tissue when it heals the muscularis propria can be replaced by scar tissue (this can narrow stomach lumen if extreme or cause pyloric stenosis, or perforation and peritonitis)
73
Extreme consequences of GI ulcers
Scar tissue build up - pyloric sphincter, peritonitis Ulcerate into liver or pancreas Haemorrhage into vessel at base- bleed into guts and cause malaena (haem component is oxidised by passing through GI tract) Extensive dramatic bleeding e.g. duodenal ulcer erodes posteriorly, Gastroduodenal artery (stomach or duodenum fill with blood, vomiting blood) Check ulcer for malignant change
74
Symptoms of gastric ulcer
Epigastric pain, back pain, burning/gnawing pain, following meals Pain at night- duodenal ulcer Food may make duodenal ulcer better as initially sphincter shuts, but once sphincter opens to release chyme it is irritated again (not always true) Resulting from bleeding- haematemesis or malaena and anemia Early satiety Weight loss
75
Management of ulcer
H Pylori- eradicate Not H pylori- stop NSAIDS or add in PPI If bleeding- endoscopic treatment, adrenaline injected, if perforated then open surgery for ulcer repair After intervention test for H pylori
76
As many gastric diseases are a result of acid damage to the mucosa, the pharmological interventions that exist target the
parietal cell at either the Proton pump or the H2 receptor Both have effect of reducing production of stomach acid

GI (22 decks)

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