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GI Tract > Gastric Physilogy > Flashcards

Gastric Physilogy Flashcards

1
Q

What are the functions of the stomach?

A

Store (before chyme enters the duodenum) and mix food

Digestion of proteins (activate pepsin) and production of chyme

Kill microbes

Secrete intrinsic factor

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2
Q

What are the key cell types of the stomach and a brief overview of their function:

A

Mucous cells - secrete an alkaline mucus that protects the stomach

Parietal cells - secrete intrinsic factor which binds to vitamin B12 which allows the terminal ileum absorption of it. Also responsible for the production of HCl

Chief cells - release pepsinogen

Enteroendocrine cells

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3
Q

What is chyme?

A

The semifluid mass of partly digested food expelled by the stomach into the duodenum.

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4
Q

How many litres of HCl are produced a day?

A

2 L

This process is energy dependent

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5
Q

How is gastric acid produced?

A

The parietal cell has a proton pump that pumps H+ into the stomach. This process requires ATP and the H+ is derived from ionised water.

K+ are pumped into the parietal cell and Cl- ions are pumped out this is to keep the charge constant.

The Cl- are replaced from the capillary with the exchange of HCO3-

The HCO3- in the cell can come from carbonic acid

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6
Q

How is gastric acid secretion switched on in the cephalic phase?

A

This is via the sympathetic nervous system (vagus nerve)

It is switched on with the sight, taste and chewing of food

Acetylcholine (ACh) is released which acts on parietal cells, causing the release of gastrin and histamine and therefore an increased acid production.

Gastrin and histamine both cause an increase in acid production by the parietal cells.

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7
Q

How is gastric acid secretion increased (gastric phase)?

A

Gastric distension and the presence of peptides causes the release of gastrin.

Gastrin directly acts on parietal cells and also causes the release of histamine, which also acts on parietal cells.

Hence there is an increase in secretion of HCl by parietal cells.

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8
Q

One final way how gastric secretion are increased?

A

Proteins in the stomach act as a buffer and mop up H+ causing pH to rise.

This leads to decreased somatostatin (inhibits parietal cell activity) and hence there is more parietal cell activity and more HCl produced.

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9
Q

How is gastric acid secretion turned off? (Gastric phase)

A

Low luminal pH (high H+)

Directly inhibits gastrin secretion

Decreased gastrin also means decreased histamine

Also stimulates somatostatin release

All of this inhibits/decrease parietal cell secretions

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10
Q

How is gastric acid secretions turned off? (Intestinal phase)

A

Duodenal distension
Low pH
Presence of a.a and fatty acids

Trigger the release of enterogastrones
Secretin — inhibits gastrin release and promotes somatostatin

Hence decrease gastric acid secretions

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11
Q 
Secretin 
Gastrin 
Somatostatin 
Histamine 
ACh

Enterogastrone

A

Enterogastrone - which inhibits the release of gastrin and promotes somatostatin and hence decrease gastric acid secretions

Gastrin - hormone that is secreted by G cells. It stimulates the secretion of gastric acid in parietal cells, also stimulates histamine secretion

Histamine - stimulates the production of gastric acid

ACh - acetylcholine - stimulates release of gastrin and histamine

Enterogastrone = An enterogastrone is any hormone secreted by the mucosa of the duodenum in response to dietary lipids

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12
Q

Overview of gastric acid secretion:

A

Controlled by = brain, stomach and duodenum

1 parasympathetic neurotransmitter ACh = + (gastrin and histamine)

1 hormone (gastrin +)

2 paracrine factors (histamine+ and somatostatin -)

2 key entergastrones (secretin - and CCK -)

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13
Q

Is in a peptic ulcer?

A

An ulcer is a breach in the mucosal surface

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14
Q

What are the causes of a stomach ulcer?

A

Helicobacter pylori

NSAIDs

Bile salts

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15
Q

How does the gastric mucosa protect itself from ulcers?

A

Mucous cells secrete alkaline mucous

Tight junctions between epithelial cells - no gastric acid into the tissues

Replacement of damaged cells

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16
Q

How does helicobacter pylori cause peptic ulcers?

A

It is a bacteria that lives in the gastric mucus and secretes urease that splits urea into CO2 and ammonia.

NH3 + H+ — NH4+

The ammonium produced as well as the proteases and vacuolating cytotoxin A damage the gastric epithelium

There is also an inflammatory response which may cause further damage.

More easy for an ulcer to form - breach the mucosa layer!

17
Q

How do NSAIDs cause peptic ulcers?

A

Non-steroidal antiinflammatory drugs

Mucus secretion is stimulated by prostaglandins cyclo-oxygenase 1 is needed for prostaglandin synthesis

NSAIDs inhibit it and hence music can not be secreted = increase change of ulcer formation

18
Q

How do bile salts cause peptic ulcers?

A

Duodeno -gastric reflux
The regurgitated bile strips away the mucus layer
Leading to reduced mucosal defence

19
Q

How to treat helicobacter pylori?

A

Proton pump inhibitor - increase pH, hostile to bacteria

Then use 2 antibiotics e.g
Amoxicillin and clarithromycin

20
Q

How to treat NSAIDs ulcers?

A

Use prostaglandin analogues - misoprostol

+ Reduce gastric acid secretion with proton pump inhibitors

21
Q

What cells produce pepsinogen and then how is pepsin produced?

A

Chief cells produce pepsinogen - due to ACh.

Pepsinogen is then converted to pepsin by HCl (pH dependent most efficient at a pH of 2) and then pepsin also catalyses this conversion (positive feedback loop)

Pepsin then acts on proteins producing smaller peptides

22
Q

Is pepsin functional in the duodenum?

A

No it is only active at a low pH - inactivated in small intestine by HCO3-

23
Q

What is the role of pepsin in digestion?

A

Not essential stomach can be removed and protein digestion can still occur.

Normally accounts for 20% of total protein digestion

24
Q

Volume of stomach when empty vs volume of stomach when full?

A

Empty = 50ml

Full 1.5L with little increase in luminal pressure

25
Q

How does receptive relaxation of the stomach take place?

A

It is mediated by the parasympathetic nervous system acting on enteric nerves plexuses

Afferent via the vagus nerve

NO and serotonin released by enteric nerves mediate relaxation…

Enteric nerves (intrinsic nerve system of the GI tract)

26
Q

After the stomach is filled then it starts chaining of the food.

What is this process?

A

Peristaltic waves begin in gastric body these are weak.

More powerful contractions in the gastric antrum take place and the pylorus closes as a peristaltic wave reaches it.

A little chyme will enter the duodenum but most forced backwards which causes it to mix/churn and hence produces chyme.

27
Q

What cause the gastric motility?

A

The interstitial cells of Cajal are responsible for the basic electrical rhythm they are found in the muscualris propria and 3 waves will take place per minute.

These pacemaker cells undergo slow depolarisation - repolarisation cycles

ACH and hormones depolarise the membranes and an action potential is produced when the threshold is reached.

The depolarisation waves transmit through the gap junctions to adjacent smooth muscle cells

28
Q

What increases the strength of the peristaltic contractions?

A

Gastrin

Gastric distension (food in stomach)

29
Q

What decreases gastric motility?

A

Duodenal luminal fat
Duodenal distension
Decrease in duodenal pH
Sympathetic nervous system - blood away from stomach - fight or flight

30
Q

What happens if you overfill the duodenum from the stomach?

A

Known as dumping syndrome - vomiting, bloating, cramps, dizziness

31
Q

What is gastroparesis?

How is it caused?

A

Delayed gastric emptying

May be caused by drugs
Parkinson’s, multiple sclerosis etc

32
Q

What drugs cause gastroparesis?

A

Gastrointestinal agents:
Aluminium hydroxide antacids
Proton pump inhibitors

Anticholinergic medication:
Benadryl
Tricyclic antidepressants

Miscellaneous:
Beta adrenergic receptor agonists
Calcium channel blockers

33
Q

Symptoms fo gastroparesis?

A

Nausea - writing food in stomach

Vomiting

Anorexia

Bloating

GI Tract (14 decks)

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