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Gastric Physiology Flashcards

(59 cards)

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1
Q

What are functions of the stomach?

A

Store and mix food
Dissolve and continue digestion
Regulate emptying into duodenum
Kill microbes
Secrete proteases
Secrete intrinsic factor
Activate proteases
Lubrication
Mucosal protection

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2
Q

What are the 4 broad types of cells in the gastric epithelium?

A

Mucous cells
Parietal cells
Chief cells
Enteroendocrine cells

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3
Q

What type of cell is found on the surface of the cell, flat epithelium?

A

Mucous secreting epithelial cells

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4
Q

What type of cells is found in the fundus of the stomach?

A

Parietal cells

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5
Q

What do parietal cells produce?

A

Hydrochloric acid
Intrinsic factor

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6
Q

What do chief cells produce?

A

Proteases

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7
Q

What do enteroendocrine cells secrete?

A

Secrete hormones

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8
Q

What does the stomach produce to break down food?

A

Hydrochloric acid

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9
Q

Describe features of gastric acid secretion

A

Approx 2 litres/day
[H+] >150mM
Secreted by parietal cells
Energy dependent - goes against conc gradient
Neurohumoral regulation

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10
Q

What acts as the pump in the regulation of gastric acid secretion?

A

H+ K+ ATPase

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11
Q

How is the gastric acid secretion process first stimulated?

A

Parasympathetic nervous system
Sight, smell, taste of food, and chewing

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12
Q

What happens in the cephalic phase (turning it on) of gastric acid secretion?

A

Acetylcholine release
ACh acts directly on parietal cells
ACh triggers release of gastrin and histamine
Net effect = increased acid production

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13
Q

What happens during the (turning on) gastric phase of gastric acid secretion?

A

Gastric distension, presence of peptides and amino acids
Gastrin release
Gastrin acts directly on parietal cells
Gastrin triggers release of histamine
Histamine acts directly on parietal cells
Net effect = increased acid production

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14
Q

What is the importance of histamine in the regulation of gastric acid secretion?

A

Helps amplify the signal that comes via the vagus nerve
Helps amplify the signal that comes from gastrin

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15
Q

How does protein in the stomach act as a stimulus to gastric acid secretion?

A

Direct stimulus for gastrin release

Proteins in the lumen act as a buffer, mopping up H+ ions, causing pH to rise:
decreased secretion of somatostatin
more parietal cell activity (lack of inhibition)

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16
Q

What happens during the turning it off (gastric phase) of gastric acid secretion?

A

Low luminal pH (high [H+])
Directly inhibits gastrin secretion
Indirectly inhibits histamine release (via gastrin)
Stimulates somatostatin release which inhibits parietal cell activity

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17
Q

What happens during the turning it off (intestinal phase) of gastric acid secretion?

A

In the duodenum:
Duodenal distension
Low luminal pH
Hypertonic luminal contents
Presence of amino acids and fatty acids

Trigger release of enterogastrones:
Secretin (inhibits gastrin release, promotes somatostatin release)
Cholecystokinin (CCK)

And short and long neural pathways, reducing ACh release

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18
Q

What parts of the body controls the regulation of gastric acid secretion?

A

Brain
Stomach
Duodenum

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19
Q

What neurotransmitter regulates the secretion of gastric acid?

A

Acetylcholine (parasympathetic)

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20
Q

What hormone regulates the secretion of gastric acid by ‘turning on the stomach’?

A

Gastrin

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21
Q

What two paracrine factors are used to regulate the secretion of gastric acid?

A

Histamine (turns stomach on)
Somatostatin (turns stomach off)

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22
Q

What two key enterogastrones allow the duodenum to communicate and turn the stomach off?

A

Secretin
CCK

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23
Q

What is a paracrine factor?

A

Sending substances which acts on neighbouring cells

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24
Q

What is a peptic ulcer?

Study These Flashcards
A

Breach in a mucosal surface caused by gastric acid

25
What are causes of peptic ulcers?
Helicobacter pylori infection Drugs – NSAIDS (aspirin, ibuprofen) Chemical irritants – alcohol, bile salts, ? Dietary factors Gastrinoma
26
How does gastric mucosa defend itself?
Alkaline mucus Tight junctions between epithelial cells Replacement of damaged cells Feedback loops
27
How does gastric mucosa defend itself?
Alkaline mucus Tight junctions between epithelial cells Replacement of damaged cells Feedback loops
28
How does helicobacter pylori cause peptic ulcers?
Lives in the gastric mucus Secretes urease, splitting urea into CO2 + ammonia Ammonia + H+ = Ammonium Ammonium, secreted proteases, phospholipases and vacuolating cytotoxin A damage gastric epithelium Inflammatory response Reduced mucosal defence
29
How do NSAIDs cause peptic ulcers?
Non-steroidal anti-inflammatory drugs Mucus secretion is stimulated by prostaglandins Cyclo-oxygenase 1 needed for prostaglandin synthesis NSAIDs inhibit cyclo-oxygenase 1 Reduced mucosal defence
30
How do bile salts cause peptic ulcers?
Duodeno-gastric reflux Regurgitated bile strips away mucus layer Reduced mucosal defence
31
How do you treat peptic ulcers caused by helicobacter pylori?
Eradicate the organism! Triple therapy: 1 proton pump inhibitor 2 antibiotics - clarithromycin - amoxicillin - tetracycline - metronidazole
32
How do you treat peptic ulcers caused by NSAID's?
Prostaglandin analogues – misoprostol Reduce acid secretion
33
How can we reduce mucosal attacks?
Turn off the protein pump Use drugs: Omeprazole, Lansoprazole, Esomeprazole
34
What drugs are used as histamine receptor antagonists?
Cimetidine Ranitidine
35
What do chief cells do?
Make proteases Produce pepsinogen (inactive enzyme precursor of pepsin) Synthesised in inactive form (zymogen) Pepsinogen mediated by input from enteric nervous system (ACh) Secretion parallels HCl secretion Luminal activation
35
What do chief cells do?
Make proteases Produce pepsinogen (inactive enzyme precursor of pepsin) Synthesised in inactive form (zymogen) Pepsinogen mediated by input from enteric nervous system (ACh) Secretion parallels HCl secretion Luminal activation
36
Where is pepsinogen activated?
Lumen of the stomach
37
What is the conversion of pepsinogen to pepsin dependent on?
pH Most efficient when pH <2 Positive feedback loop (Pepsin also catalyses the reaction) Pepsin only active at low pH. Irreversible inactivation in small intestine by HCO3-
38
How does HCl aid in the conversion of pepsinogen to pepsin?
HCl cleaves pepsingogen
39
Why do we secrete pepsinogen and not pepsin?
We don't want pepsin to digest our own cells
40
What is the role of pepsin in protein digestion?
Not essential (protein digestion can occur if the stomach is removed) Accelerates protein digestion Normally accounts for ~20% of total protein digestion Breaks down collagen in meat – helps shred meat into smaller pieces with greater surface area for digestion
41
What is the volume of an empty stomach?
~50mL
42
What is the volume of the stomach when eating?
When eating, can accommodate ~1.5L with little increase in luminal pressure
43
What happens to the smooth muscle in body and fundus during gastric motility?
Undergoes receptive relaxation
44
What is receptive relaxation of the smooth muscle in body and fundus mediated by?
Mediated by parasympathetic nervous system acting on enteric nerve plexuses Coordination – afferent input via Vagus nerve Nitric oxide and serotonin released by enteric nerves mediate relaxation
45
What is peristalsis?
Coordinated contractions in stomach starting from the fundus Peristaltic waves begin in gastric body Weak contraction in body (little mixing) More powerful contraction in gastric antrum Pylorus closes as peristaltic wave reaches it Little chyme enters duodenum Antral contents forced back towards body (mixing
46
Where is the more powerful contraction in stomach?
Gastric antrum
47
What happens to the pylorus when the peristaltic wave reaches it?
Closes
48
What is the frequency of peristaltic waves determined by?
Determined by pacemaker cells in muscularis propria and is constant (3/minute) Interstitial cells of Cajal Pacemaker cells undergo slow depolarisation-repolarisation cycles
49
What are the depolarisation waves from intersitial cells of cajal transmitted through?
Gap junctions to adjacent smooth muscle cells Do not cause significant contraction in empty stomach
50
What hormone turns on peristalsis?
Gastrin
51
What is the strength of peristaltic contractions increased by?
Gastrin Gastric distension (medicated by mechanoreceptors)
52
What is the strength of peristaltic contractions decreased by?
Duodenal distension Increase in duodenal luminal fat Increase in duodenal osmolarity Decrease in duodenal luminal pH Increase in sympathetic NS action Decrease in parasympathetic NS action
53
What does the overfilling of duodenum by a hypertonic solution cause?
Dumping syndrome: Vomiting, bloating, cramps, diarrhoea, dizziness, fatigue, weakness, sweating
54
Why do we need to control gastric emptying?
Capacity of stomach > capacity of duodenum Duodenum cannot undergo receptive relaxation
55
What is gastroparesis?
Delayed gastric emptying
56
What are causes of gastroparesis?
Idiopathic - don't know Autonomic neuropathies (e.g. in Diabetes mellitus) - damage to vagus nerve Drugs Abdominal surgery - touching intestines stops them from moving Parkinson’s disease Multiple sclerosis Scleroderma - connective tissue disease Amyloidosis Female gender - more common in females
57
What drugs can cause gastroparesis?
Gastrointestinal agents: Aluminium hydroxide antacids H2 receptor antagonists Proton pump inhibitors Sucralfate Anticholinergic medications Diphenhydramine (Benadryl) Opioid analgesics Tricyclic antidepressants Miscellaneous Beta-adrenergic receptor agonists Calcium channel blockers Interferon alpha Levodopa
58
What are symptoms of gastroparesis?
Nausea Early satiety Vomiting undigested food (looks like faeces) GORD Abdo pain/bloating Anorexia

GastroIntestinal (19 decks)

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