5-Pathology of stomach

Question 1

Describe the basic cell structure in the stomach

Answer 1

Columnar epithelial cells cover surface and extend into gastric pits and glands where secretary cells are found:
Parietal 
Chief
G
Mucous

Question 2

Relate the shape of the stomach to its function

Answer 2

Large to small

Causes contents to accelerate, separating contents so lumps are left behind and liquid chyme is ejected into duodenum

Question 3

Describe the smooth muscle in the stomach

Answer 3

Upper stomach: Sustained contractions create basal tone

Lower stomach: Strong peristalsis, contractions every 20 secs from proximal to distal, mixes stomach contents

Question 4

What is receptive relaxation?

Answer 4

Vagually mediated relaxation of proximal stomach
Rugae allow stomach to distend, so food can enter without raising intra-gastric pressure too much and prevents reflux of stomach contents during swallowing

Question 5

What are the secretary cells in the stomach and what do they produce?

Answer 5

Parietal cell - HCl and intrinsic factor (needed for reabsorption of vit b12)
G cell - Gastrin
Enterochromaffin like cell - Histamine
Chief cell - pepsinogen (activated by acid to pepsin)
D cell - Somatostatin (inhibits acid release)
Mucous cell - Mucous

Question 6

What is predominantly secreted from the different areas of the stomach?

Answer 6

Cardia - mucus
Fundus/body - Mucus, HCl (parietal) and pepsinogen (chief)
Pylorus - Gastrin (g) and somatostatin (D)

Question 7

In the gastric pits and glands, what order do the secretory cells appear?

Answer 7

Pit: Surface mucous cells
Gland: Mucous neck cells
Parietal 
Chief
Enterondocrine (G and D)

Question 8

How is HCl production controlled?

Answer 8

Parietal cells stimulated by:
ACh - Vagal parasympathetic stimulation releases ACh which binds to muscarinic receptor Histamine- Enterochromaffin like cell releases histamine, binds to H2 (histamine) receptor
Gastrin - Gastrin in blood stream binds to cholecystikinin receptor

Question 9

Describe how gastrin secretion is controlled

Answer 9

G cells stimulated by:
Peptides/amino acids in stomach lumen
Breakdown of proteins stimulates Gastrin releasing peptide, stimulates G cell
Sight/smell of food stimulates vagus nerve, which causes release of ACh, binds to muscarinic receptor
Inhibited by:
Gastrin release stimulates parietal cell to release somatostatin, which binds to somatostatin receptor

Question 10

Describe how HCl production is inhibited

Answer 10

Food acts a buffer, when it leaves stomach pH drops
D cells detect lower pH, release somatostatin
Somatostatin travels in blood stream to bind to s receptors on G cells, blocking gastrin release. Gastrin no longer binds to cholecystikinin receptor on parietal cell, so H+ production not stimulated
Somatostatin binds to s receptors on enterochromaffin like cell, blocking histamine release, so histamine doesn’t bind to H2 receptors on parietal cell, so H+ production not stimulated

Question 11

Why is blood leaving the stomach a higher pH?

Answer 11

Anion antiporter, pumps HCO3- out of stomach lumen to let in Cl- to form HCl

Question 12

What are the phases of digestion?

Answer 12

Cephalic
Gastric
Intestinal

Question 13

Describe the cephalic phase of digestion

Answer 13

Parasympathetic stimuli such as smelling/chewing food causes the vagus nerve to directly stimulate parietal cells and indirectly stimulate G cells by releasing GRP
Increases gastric motility

Question 14

Describe the gastric phase of digestion

Answer 14

Stomach distends, stimulating the vagus nerve which then stimulates parietal and G cells
Presence of amino acids stimulates G cells
Food acts a buffer so removes inhibition of gastrin production
Enteric nervous system and gatrin cause smooth muscle contractions to mix and break down the food

Question 15

Describe the intestinal phase of digestion

Answer 15

Amino acids in duodenum initially stimulate G cell secretion
But, presence of lipids activates enterogastric reflex, reduces vagal stimulation
Chyme stimulates CCK and secretin to help suppress secretion

Question 16

What are the stomach’s defences against HCl?

Answer 16

Mucous and HCO3, released by surface and neck mucous cells
High turn over of epithelial cells due to presence of stem cells, keeps epithelia intact
Prostaglandins, maintain mucosal blood flow supplying epithelium with nutrients

Question 17

What can breach the stomach’s defences against HCl?

Answer 17

Alcohol - dissolves the mucus layer
Helicobacter pylori - chronic gastritis, inflammation and damage to mucosal cells
NSAIDS - inhibit prostaglandins

Question 18

Define dyspepsia

Answer 18

Upper GI discomfort

Question 19

What is gastro oesophageal reflux disease?

Answer 19

Chronic reflux of stomach contents into the oesophagus

Question 20

What can cause GORD?

Answer 20

Lower oesophageal sphincter problems 
Delayed gastric emptying, raising intra-gastric pressure 
Hiatus hernia (LOS)
Obesity, raising intrabdominal pressure

Question 21

What are the risks associated with GORD?

Answer 21

Oesophagitis (inflam)
Strictures
Barrett’s oesophagus (squamous epithelium to columnar), risk of adenocarcinoma

Question 22

How is GORD treated?

Answer 22

Lifestyle modifications - lose weight, decrease intrabdominal pressure, eat earlier, so food digested before lying down
Pharmalogical:
Antacids - form layer on acid, less likely to reflux
H2 antagonists
PPIs- Proton pump inhibitors stop parietal cells

Question 23

What are the causes of acute gastritis?

Answer 23

Heavy use of NSAIDs
Alcohol
Chemotherapy
Bile reflux

Question 24

What are the causes of chronic gastritis?

Answer 24

H-pylori infection
Antibodies to gastric parietal cells
Chronic alcohol abuse/NSAIDS

Question 25

What are the symptoms of chronic gastritis?

Answer 25

H-pylori: Asymptomatic or peptic ulcers, adenocarcinoma, MALT lymphoma (mucosal associated lymph tissue)
Autoimmune: Anaemia (parietal cells damaged, normally produce intrinsic factor for vit b12 reabsorption)
Glossitis (big red tongue)
Anorexia

Question 26

What is peptic ulcer disease?

Answer 26

Defects in gastric/duodenal mucosa, extending through muscularis mucosa

Question 27

Where are peptic ulcers commonly found and why?

Answer 27

Lesser curve of stomach due to blood flow conditions

Proximal duodenum due to its exposure to stomach acid

Question 28

What causes peptic ulcer disease?

Answer 28

Mucosal injury:
Stomach acid
H-pylori
NSAIDs

Question 29

What are the symptoms of peptic ulcer disease?

Answer 29

Epigastric (and sometimes back) pain
Burning pain following meals and at night
Anaemia/bleeding 
Satiety (loss of appetite) 
Weight loss

Question 30

What pharmacological intervention is given to patients with gastric disease?

Answer 30

H2 blockers to prevent histamine binding to H2 receptors and stimulating parietal cells to produce H+
Cimetidine and Ranitidine
PPIs to block H+ pump in parietal cells
Omeprazole

Question 31

Describe H-pylori

Answer 31

Spread orally or faecal-orally
Gram negative (pink), slightly curved lines
Flagellum gives good motility so it can adhere to gastric epithelia

Question 32

What makes H-pylori dangerous?

Answer 32

Releases cytotoxins - direct epithelial injury
Produces urease, converting urea to ammonium which is toxic to epithelia
Degrades mucus layer
Promotes inflammatory response, resulting in self injury

Question 33

What are the symptoms of H pylori colonisation in different areas of the stomach?

Answer 33

Antrum - Duodenal ulceration
Antrum and body - asymptomatic
Body - Cancer

Question 34

What do the different areas of the stomach primarily secrete?

Answer 34

Fundus and Cardia: 
Mucous- Mucous cells 
Body:
HCl and intrinsic factor - parietal cells
Pepsinogen - chief cells
Antrum:
Gastrin - G cells

Question 35

What is stress ulceration?

Answer 35

Gastritis/ulceration following:
Severe burns
Raised intracrainal pressure
Sepsis 
Trauma