Upper GI Disorders: Mouth + Oesophagus

Question 1

What is the GI tract made up of?

Answer 1

Mouth
Oesophagus
Stomach
Pancreas
Small intestine
Large intestine
Liver

Question 2

What are the main GI disorders?

Answer 2

Gastro oesophageal reflux disease (GORD)
Peptic ulcer disease (PUD)

Question 3

What is an oral ulceration?

Answer 3

Break in oral epithelium

Question 4

What is oral ulceration caused by?

Answer 4

Physical or chemical injury
Drugs

Question 5

What is stomatitis?

Answer 5

Inflammation of lining of any of soft-tissues of mouth

Question 6

What is stomatitis caused by?

Answer 6

Poor oral hygiene
Poorly fitted dentures

Question 7

What is leukoplakia?

Answer 7

Painless white patches on side of tongue/cheek

Question 8

What is oesophagus made up of?

Answer 8

Upper oesophageal sphincter
Oesophageal body
Lower oesophageal sphincter
Diaphragm

Question 9

What does the UOS prevent?

Answer 9

Air entering oesophagus + reflux

Question 10

What does LOS prevent?

Answer 10

Reflux

Question 11

What is GORD?

Answer 11

Exposure of unprotected oesophageal epithelium to acid

Question 12

What is the stomach made up of?

Answer 12

Fundus
Body
Pylorus

Question 13

What is present at body of stomach?

Answer 13

Parietal cells (HCl)
Mucous cells
Chief cells

Question 14

What is present at pylorus of stomach?

Answer 14

Mucous cells
G cells
D cells
NO ACID SECRETING CELLS

Question 15

What is aspirin used for?

Answer 15

Pain killer
Blood thinner

Question 16

Describe how parietal cells secrete acid

Answer 16

Resting cell H+/K+-ATPase in cytoplasmic vesicles
Stimulated cell H+/K+-ATPase membrane fused
Increase SA + membrane pumps

Question 17

What are the positive regulators of parietal cell?
(Stimulate to release acid)

Answer 17

Acetylcholine
Histamine
Gastrin

Question 18

What is the negative regulator of parietal cell?

Answer 18

Somatostatin

Question 19

Describe acetylcholine positive regulator

Answer 19

Enteric neurons released from
Direct parietal cell stimulation

Question 20

Describe histamine positive regulator

Answer 20

ECL cells
Direct parietal cell stimulation
Paracrine activity

Question 21

Describe gastrin positive regulator

Answer 21

G cells
Endocrine action
Stimulate histamine release
Directly stimulates parietal cell proliferation

Question 22

Describe somatostatin negative regulator

Answer 22

D cells
Directly inhibits parietal cell secretion
Inhibits gastrin + histamine release

Question 23

What is the Ach receptor in acid secretion pathway?

Answer 23

Muscarinic M3 receptor

Question 24

What is the histamine receptor in acid secretion pathway?

Answer 24

H2

Question 25

What is gastrin receptor in acid secretion pathway?

Answer 25

CKKB/CCK2 receptor

Question 26

What does Ach + gastrin act through in acid secretion pathway?

Answer 26

G-coupled receptors Increase Ca2+ + diacylglycerol Through PLC-inositol 1,4,5-triphosphate (IP3) pathway

Question 27

What does histamine act through in acid secretion pathway?

Answer 27

G-coupled receptors Increase cAMP

Question 28

What gastrin + Ach dependent on?

Answer 28

Ca2+

Question 29

What is histamine dependent on?

Answer 29

cAMP

Question 30

What are the 3 stages of acid secretion stimulation?

Answer 30

Cephalic phase Gastric phase Intestinal phase

Question 31

Describe cephalic phase 1

Answer 31

Sight/smell/ thought food

Question 32

Describe gastric phase 2

Answer 32

Food in stomach Mechanoreceptor neural reflex Peptides in food stimulate G cells = gastrin Food increase pH = prevent D cell activity

Question 33

Describe intestinal phase 3

Answer 33

Chyme enter duodenum Feedback prevent chyme acidity Duodenal stimulation of hormones Decrease food, decrease pH = stimulates D cell activity

Question 34

What happens to gastric secretion following food?

Answer 34

Food in stomach buffers acid + raises pH Suppresses D cells Gastrin + HCl released Stomach distention, digestion triggers secretion vol + HCl Food leaves stomach = acid increases = pH falls = D cells stimulated = somatostatin inhibits HCl production

Question 35

How is HCl secretion controlled?

Answer 35

Direct stimulation of ECL Direct stimulation of G cells Inhibition of somatostatin Pyloric antrum exposure to peptides

Question 36

Describe the mechanism of HCl secretion

Answer 36

CO2 diffuses into parietal cell Hydrated to carbonic acid by carbonic hydrase H2CO3 dissociated to H+ + H2CO3- H+/K+-ATPase actively transport H+ out, K+ in Na+ actively reabsorbed K+ recycles to gastric lumen via K+ channel Cl- exits passively from cells via Cl- channel

Question 37

What are the protective functions of prostaglandin acid regulation?

Answer 37

Increase mucus secretion Increase cell regeneration Increase HCO3- release Increase H+ secretion Increase blood flow

Question 38

What is present to protect against acid?

Answer 38

Intrinsic mucosal protection