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GastroIntestinal > Gastric Physiology > Flashcards

Gastric Physiology Flashcards

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?

A

Breach in a mucosal surface caused by gastric acid

25
Q

What are causes of peptic ulcers?

A

Helicobacter pylori infection
Drugs – NSAIDS (aspirin, ibuprofen)
Chemical irritants – alcohol, bile salts, ? Dietary factors
Gastrinoma

26
Q

How does gastric mucosa defend itself?

A

Alkaline mucus
Tight junctions between epithelial cells
Replacement of damaged cells
Feedback loops

27
Q

How does gastric mucosa defend itself?

A

Alkaline mucus
Tight junctions between epithelial cells
Replacement of damaged cells
Feedback loops

28
Q

How does helicobacter pylori cause peptic ulcers?

A

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
Q

How do NSAIDs cause peptic ulcers?

A

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
Q

How do bile salts cause peptic ulcers?

A

Duodeno-gastric reflux
Regurgitated bile strips away mucus layer
Reduced mucosal defence

31
Q

How do you treat peptic ulcers caused by helicobacter pylori?

A

Eradicate the organism!
Triple therapy:
1 proton pump inhibitor

2 antibiotics
- clarithromycin
- amoxicillin
- tetracycline
- metronidazole

32
Q

How do you treat peptic ulcers caused by NSAID’s?

A

Prostaglandin analogues – misoprostol
Reduce acid secretion

33
Q

How can we reduce mucosal attacks?

A

Turn off the protein pump
Use drugs: Omeprazole, Lansoprazole, Esomeprazole

34
Q

What drugs are used as histamine receptor antagonists?

A

Cimetidine
Ranitidine

35
Q

What do chief cells do?

A

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
Q

What do chief cells do?

A

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
Q

Where is pepsinogen activated?

A

Lumen of the stomach

37
Q

What is the conversion of pepsinogen to pepsin dependent on?

A

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
Q

How does HCl aid in the conversion of pepsinogen to pepsin?

A

HCl cleaves pepsingogen

39
Q

Why do we secrete pepsinogen and not pepsin?

A

We don’t want pepsin to digest our own cells

40
Q

What is the role of pepsin in protein digestion?

A

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
Q

What is the volume of an empty stomach?

A

~50mL

42
Q

What is the volume of the stomach when eating?

A

When eating, can accommodate ~1.5L with little increase in luminal pressure

43
Q

What happens to the smooth muscle in body and fundus during gastric motility?

A

Undergoes receptive relaxation

44
Q

What is receptive relaxation of the smooth muscle in body and fundus mediated by?

A

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
Q

What is peristalsis?

A

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
Q

Where is the more powerful contraction in stomach?

A

Gastric antrum

47
Q

What happens to the pylorus when the peristaltic wave reaches it?

A

Closes

48
Q

What is the frequency of peristaltic waves determined by?

A

Determined by pacemaker cells in muscularis propria and is constant (3/minute)
Interstitial cells of Cajal

Pacemaker cells undergo slow depolarisation-repolarisation cycles

49
Q

What are the depolarisation waves from intersitial cells of cajal transmitted through?

A

Gap junctions to adjacent smooth muscle cells

Do not cause significant contraction in empty stomach

50
Q

What hormone turns on peristalsis?

A

Gastrin

51
Q

What is the strength of peristaltic contractions increased by?

A

Gastrin
Gastric distension (medicated by mechanoreceptors)

52
Q

What is the strength of peristaltic contractions decreased by?

A

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
Q

What does the overfilling of duodenum by a hypertonic solution cause?

A

Dumping syndrome: Vomiting, bloating, cramps, diarrhoea, dizziness, fatigue, weakness, sweating

54
Q

Why do we need to control gastric emptying?

A

Capacity of stomach > capacity of duodenum

Duodenum cannot undergo receptive relaxation

55
Q

What is gastroparesis?

A

Delayed gastric emptying

56
Q

What are causes of gastroparesis?

A

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
Q

What drugs can cause gastroparesis?

A

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
Q

What are symptoms of gastroparesis?

A

Nausea
Early satiety
Vomiting undigested food (looks like faeces)
GORD
Abdo pain/bloating
Anorexia

GastroIntestinal (19 decks)

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