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
Q

Intestinal Phase

A

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
Q

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

A

due to HCl

-also stimulate pancreas and bile ducts to release HCO3

27
Q

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

A

due to partially digested fats and proteins.

-also stimulate release of pancreatic enzymes and gallbladder contraction to release bile to digest the fats

28
Q

What does Helicobacter pylori cause?

A
  • Gastritis (non-specific inflammation post infection)
  • Peptic Ulcer
  • gastric cancer
  • Gastric MALToma - lymphoid tissue lymphoma cancer
29
Q

Who does H.pylori infect and where?

A

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
Q

Treatment for H.pylori

A

‘triple therapy’ as single AB doesn’t work

  • omeprazole, clarithromycin and amoxycillin for 14 days
  • is resistance, 2nd regime
31
Q

Causes of Peptic Ulcer Disease (stomach or duodenum)

A

Mainly H.pylori and aspirin and NSAIDs

32
Q

How did they initially treat peptic ulcers

A

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

33
Q

Symptoms of peptic ulcers

A

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

34
Q

2 main types of Gastric Cancer

A

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
Q

How does H.pylori affect gastric cancer

A

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