Gastric Digestion and Disease Flashcards

1
Q

Functions of the stomach

A
  • 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)
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2
Q

What is required to have normal function of gastric emptying

A
  • intact atrum, pylorus and duodenum
  • Normal vagal function to co-ord activity
  • normal hormonal function
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3
Q

How does food move through the stomach?

A

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)

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4
Q

Abnormal Gastric emptying

A

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

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5
Q

Role of Gatric Acid

A

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

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6
Q

Dumping syndrome is?

A

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

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7
Q

Achlorhydria

A

absent or low gastric acid, often related to pernicious anaemia

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8
Q

How is acid secreted in the stomach?

A

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

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9
Q

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

A

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

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10
Q

H20 + CO2&raquo_space; H+ + HCO3

is catalysed by what enzyme

A

carbonic anhydrase

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11
Q

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

A

because pH and osmolarity need to stay in equilibrium.

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12
Q

How exactly does the parietal cells secrete acid?

A

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

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13
Q

Protective factors of the gastric mucosa?

What happens if these protective factors results in?

A

Mucus layer
Bicarbonate secretion

Damage to these = ulceration

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14
Q

ECL cells are?

A

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

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15
Q

G cells

A

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

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16
Q

D cells

A

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

17
Q

ACh

A

neurotransmitter, released by vagus and enteric neurons

Stimulates parietal, ECL and gastrin cells

18
Q

Abnormal Gastric Secretion

A

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
Q

What are other gastric secretions

A
  • pepsinogen
  • Intrinsic Factor
  • Prostaglandins
20
Q

Pepsinogen?

A

from Chief cells
cleaved to form pepsin
pepsin degrades protein

21
Q

Intrinsic Factor?

A

Parietal cells

B12 absorbtion

22
Q

Prostaglandins

A

Lipid molecules to repair mucosa due to acid damage

23
Q

Celiac phase

A

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

24
Q

Gastric phase

A
  • 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