Gastric Digestion and Disease Flashcards Preview

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Flashcards in Gastric Digestion and Disease Deck (35):
1

Functions of the stomach

- food reservoir
-food digestion (antrum mixes/grinds)
-controls passage of food to SI (pylorus regulates size/timing)
-Gastric acid secretion (+ other secretions for protection against acid)

2

What is required to have normal function of gastric emptying

-intact atrum, pylorus and duodenum
-Normal vagal function to co-ord activity
-normal hormonal function

3

How does food move through the stomach?

1- Fundus (storage) relaxes when food is about to enter, (vagus nerve), causing reflex
2- body & antrum contract together allowing food to be moved to the distal stomach
3- Pylorus is contracted (stops spillage)
4- mixing of food in antrum (retropulsion)

4

Abnormal Gastric emptying

Rapid GE: common post-gastric surgery, when antrum/pylorus removed> "dumping Syndrome"
Delayed GE: eg) diabetic gastroparesis due to vagal nerve damage, usually due to ANS neuropathy

5

Role of Gatric Acid

main role is to sterilise food, make the stomach environment hostile to bacteria (par H.pylori)

6

Dumping syndrome is?

nausea vomiting cramping, poop as food moves too fast stomach > duodenum, food not completely digested.
-Hyperosmolar chyme = fluid shift = intestinal distention = pain =diarrhoea

7

Achlorhydria

absent or low gastric acid, often related to pernicious anaemia

8

How is acid secreted in the stomach?

Parietal cells. Located in the body, with proton pumps to secrete HCL. Secrete ~2L/day

9

how does the H/K ATPase pump in the Parietal cells work and what is it for

A proton pump that actively pumps H+ from cells into stomach
H20 + CO2 >> H+ + HCO3
in exchange K enters cell, HCO3 transported out of cell into bloodstream exchanged with Cl-.
Requires ATP

10

H20 + CO2 >> H+ + HCO3
is catalysed by what enzyme

carbonic anhydrase

11

Why does HCO3 swap for Cl- and H+ swap for K+

because pH and osmolarity need to stay in equilibrium.

12

How exactly does the parietal cells secrete acid?

Tubovesicles fuse with canaliculus, increased SA and proton pump numbers increase acid secretion into lumen and gut, against a 3 mill fold conc gradient

13

Protective factors of the gastric mucosa?
What happens if these protective factors results in?

Mucus layer
Bicarbonate secretion

Damage to these = ulceration

14

ECL cells are?

Enterochromaffin-like cells
-located body of stomach, secrete histamine (paracrine activity)
Stimulates acid secretion from adjacent parietal cells

15

G cells

antrum of stomach
secrete gastrin
endocrine activity
(enters blood circ. binds to ECL, > histamine release > HCL release)

16

D cells

antrum of stomach
secrete somatostatin
endocrine & paracrine
inhibits acid secretion by acting on adjacent G cells

17

ACh

neurotransmitter, released by vagus and enteric neurons
Stimulates parietal, ECL and gastrin cells

18

Abnormal Gastric Secretion

Increased : 'Gastrinoma', cancer with tumours that produce gastrin> ulcers and destruction of gastric mucosa
Decreased:
-'Pernicious anaemia' AB against parietal cells and/or IF
-gastric surgey, body or antrum removed
-vagotomy: loss of vagus nerve > less ACh
-drugs

19

What are other gastric secretions

-pepsinogen
-Intrinsic Factor
-Prostaglandins

20

Pepsinogen?

from Chief cells
cleaved to form pepsin
pepsin degrades protein

21

Intrinsic Factor?

Parietal cells
B12 absorbtion

22

Prostaglandins

Lipid molecules to repair mucosa due to acid damage

23

Celiac phase

think/see/smell food
brain stimulates vagus/enteric nerve
ACh release
Parietal, HCL and G cells released

24

Gastric phase

-when food starts to enter the stomach
-physical digestion + AA release (stimulate G cells)
-food causes distention, stimulates enteric nerves > ACh > parietal, ECL and G

25

Intestinal Phase

too much acid in stomach, time to turn off acid secretion
- Excessive HCl > D cells
-somatostatin release
-G cells inhibited (stopping HCl)

also
- Fats + HCl in duodenum release 'secretin' & 'cholecystokinin
-inhibit cid secretion

26

Why is Secretin released. extra job other then inhibiting acid secretion?

due to HCl
-also stimulate pancreas and bile ducts to release HCO3

27

Why is cholecystokinin. Extra job other then inhibiting acid secretion?

due to partially digested fats and proteins.
-also stimulate release of pancreatic enzymes and gallbladder contraction to release bile to digest the fats

28

What does Helicobacter pylori cause?

-Gastritis (non-specific inflammation post infection)
-Peptic Ulcer
-gastric cancer
-Gastric MALToma - lymphoid tissue lymphoma cancer

29

Who does H.pylori infect and where?

Only humans in the antrum of the stomach. Via person-to-person transmission (oral-oral or faecal-oral)
Tends to be childhood infection (1-5 yrs), and is caused by living conditions, ethnic group, country of birth

30

Treatment for H.pylori

'triple therapy' as single AB doesn't work
-omeprazole, clarithromycin and amoxycillin for 14 days
-is resistance, 2nd regime

31

Causes of Peptic Ulcer Disease (stomach or duodenum)

Mainly H.pylori and aspirin and NSAIDs

32

How did they initially treat peptic ulcers

gastrectomy (remove antrum)
Vagotomy (part of vagus nerve)
Pyloroplasty: cut and resuture pylorus

33

Symptoms of peptic ulcers

non-specific epigastric pain
bleeding
perforation
obstruction due to scarring/fibrosis

34

2 main types of Gastric Cancer

1) Intestinal : well differentiated and cells arranged in a tubular/glandular pattern
2) Diffuse: Poorly differentiated cells, lack of glandular formation. Can infiltrate gastric wall

35

How does H.pylori affect gastric cancer

Can produce widespread inflammation of gastric mucosa and destruction of parietal cells > low acid (achlorydria) > bacterial overgrowth > carcinogens