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Gastrointestinal > Physiology and Pharmacology of Salivary and Gastric Secretion and Gastric Motility > Flashcards

Physiology and Pharmacology of Salivary and Gastric Secretion and Gastric Motility Flashcards

1
Q

Name the three pairs of salivary glands in the head

A

Parotid
Submandibular
Sublingual

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2
Q

What are the functions of saliva?

A

Lubrication (important for speech and swallowing)
Solvent (taste)
Antibacterial
Digestion of complex carbohydrate (amylase)
Neutralization of acid (bicarbonate)
Facilitates sucking by infants (fluid seal)

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3
Q

Name some of the constiuents of saliva

A

Lysozyme, lactoferrin, immunoglobulins, amylase and bicarbonate

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4
Q

What are the two stages of saliva formation?

A

Primary secretion and secondary modification

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5
Q

Where does the primary secretion take place?

A

Acinus

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6
Q

What does the primary secretion contain?

A

Na+, K+, Cl-, HCO3-, mucus and amylase

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7
Q

Where does secondary modification of saliva take place?

A

Duct cells

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8
Q

How is saliva modified?

A

Na+ and Cl- is removed, K+ and HCO3- is added, there is no movement of water (dilution)

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9
Q

Where does the dilution of saliva take place?

A

As it passes through the duct cells

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10
Q

What aspect of saliva composition allows the detection of salty taste?

A

NaCl content is much lower than plasma

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11
Q

What aspect of saliva allows the detection of sweet taste?

A

No glucose

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12
Q

What two reflexes increase the rate of saliva formation?

A

Simple reflex

Conditioned reflex

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13
Q

What is the simple relex?

A

Chemo or pressure receptors in the mouth are activated in the presence of food or other stimulus
Impulses are sent via afferent nerves to salivary centre in the medulla

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14
Q

What is the conditioned reflex?

A

Think about, smell, see, hear preparation of food

Cerebral cortex sends messages to the salivary centre in the medulla

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15
Q

What happens once signals have reached the salivary centre in the medulla?

A

Impulses are sent via extrinsic autonomic nerves

(sympathetic and parasympathetic stimulation) to the salivary glands, which then increase production

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16
Q

Does sympathetic or parasympathetic stimulation have a more dominant role in saliva production?

A

Parasympathetic

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17
Q

What nerves are involved in the parasympathetic stimulation for saliva production?

A

Glossopharyngeal and facial nerves

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18
Q

What type of saliva does parasympathetic stimulation result in?

A

Large volume, watery, enzyme rich

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19
Q

What receptors are involved in the parasympathetic stimulation?

A

M3 muscarinic acetlycholine receptors

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20
Q

When is the sympathetic stimulation of salivary glands present?

A

During stressful situations

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21
Q

What nerve fibers are involved in sympathetic stimulation?

A

Postganglionic fibres from superior cervical ganglia

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22
Q

What type of saliva results from sympathetic stimulation?

A

Small volume, thick, mucus rich

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23
Q

What receptors are involved in sympathetic stimulation?

A

B1-adrenoceptors

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24
Q

What are the names of the different parts of the stomach?

A

Fundus
Body
Antrum

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25
Q

What are the functions of the stomach?

A

Starting point for protein digestion
Mixes food with gastric secretions to produce chyme
Limited amount of absorption
Stores food before passing it into the small intestine as chyme for further digestion and absorption

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26
Q

How is the food emptied from the stomach?

A

Waves of peristaltic contraction push the food

The strength of antral waves determine the escape of chyme through the pyloric sphincter

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27
Q

What factors govern the strength of the antral waves?

A

Gastric and duodenal factors

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28
Q

What are the gastric factors that influence stomach emptying?

A

The rate of emptying is proportional to the volume of chyme in the stomach
Distension increases motility

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29
Q

How can the duodenum delay gastric emptying through neural response?

A

Enterogastric reflex -

Signals from intrinsic nerve plexuses and autonomic nervous system decrease antral peristalic activity

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30
Q

How can the duodenum delay gastric emptying through hormonal response?

A

Release of enterogastrones from the duodenum inhibits stomach contraction

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31
Q

What stimuli within the duodenum drive the neuronal and hormone responses?

A

Fat
Acid
Hypertonicity
Distension

32
Q

What is the name of the neck of the gastric glands?

A

Gastric pIt

33
Q

Where do the gastric glands lie?

A

In the mucosa

34
Q

Name the 2 different cell types in the gastric glands in the pyloric gland area

A

D cell

G cell

35
Q

What do each of the cells secrete?

A

D cells - somatostatin

G cells - gastrin

36
Q

Where is the pyloric gland area?

A

The antrum

37
Q

Name the 3 different cell types in the gastric glands in the oxyntic mucosa

A

Chief cell
Enterochromaffin-like cell
Parietal cell

38
Q

What do each of the cells secrete?

A

Chief cells - pepsinogen
Enterochromaffin-like cells - histamine
Parietal cells - hydrochloric acid and intrinsic factor

39
Q

Where is the oxyntic mucosa?

A

The fundus and body

40
Q

In the pyloric gland area, what is the function of gastrin?

A

Stimulates HCl secretion

41
Q

n the pyloric gland area, what is the function of somatostatin?

A

Inhibits HCl secretion

42
Q

n the pyloric gland area, what is the function of mucus?

A

Protective

43
Q

In the oxyntic mucosa what is the function of HCl?

A

Activates pepsinogen to pepsin
Denatures proteins
Kills most micro-organisms ingested with food

44
Q

In the oxyntic mucosa what is the function of pepsinogen?

A

Inactive precursor of the peptidase, pepsin

45
Q

In the oxyntic mucosa what is the function of instrinsic factor?

A

Binds vitamin B12 allowing absorption in terminal ileum

46
Q

Explain the autocatalytic effect of pepsin

A

HCl converts pepsinogen to pepsin. Pepsin then activates pepsinogen

47
Q

What are the three stages of gastric secretion?

A

Cephalic
Gastric
Intestinal

48
Q

When is the cephalic phase of gastric secretion?

A

Before food reaches the stomach

49
Q

When is the gastric phase of gastric secretion?

A

When food is in then stomach

50
Q

When is intestinal stage of gastric secretion?

A

After food has left the stomach

51
Q

What is the function of the cephalic stage of gastric secretion?

A

It prepares the stomach to receive food

52
Q

What two neurotransmitters are involved in vagal stimulation of the enteric nervous system?

A

Acetylcholine

Gastrin releasing peptide

53
Q

What is the gastric stage of gastric secretion?

A

Chemical and mechanical factors augment secretion

54
Q

What is the intestinal phase of secretion?

A

Factors originating from the small intestine switch off acid secretion

55
Q

What happens to stimulation of somatostatin when the stomach is full?

A

It is inhibited

56
Q

What are the drug classes that influence acid secretion?

A

Muscarinoc receptor antagonists
Proton-pump inhibitors
Non-steriodal anti-inflammatory drugs
H2 histamine receptor antsgonists

57
Q

How do muscarinic receptor antagonists influence acid secretion?

A

They competively block the M1 and M3 receptors meaning that AcH doesn’t have an affect

58
Q

Give an example of a muscarinic receptor antagonist

A

Pirenzepine

59
Q

How do proton-pump inhibitors work?

A

They block the H+/K+- dependent proton pump of cells by covalent modification
They are delivered via the systemic circulation

60
Q

What is an example pf a proton pump inhibitor?

A

Omaprazole

61
Q

How do NSAIDs work?

A

They block reversibility

62
Q

Give an example of an NSAID

63
Q

How do histamine receptor antagonists work?

A

They competitively block the histamine receptor reducing acid secretion

64
Q

Give an example of a H2 histamine receptor antagonist

A

Ranitidine

65
Q

What protects the mucosa from attack by HCI and pepsin?

A

A thick mucus gel layer above the apical surface of the mucosa cell

66
Q

What is released into the muscus layer to neutrilise it?

A

Bicarbonate

67
Q

What is a peptic ulcer?

A

An ulcer in an area where the mucosa is exposed to hydrocholric acid and pepsin

68
Q

How can NSAIDs cause gastric ulcers or bleeding

A

They reduce prostaglandin formation

69
Q

How can gastric ulcer formation from long term use of NSAIDs be prevented?

A

Stable PGE1 analogue e.g. misoprostol

70
Q

Chronic infection of the gastric antrum from what bacteria causes development of peptic ulcers?

A

Helicobacter pylori

71
Q

How does infection from helicobacter pylori result in the formation of peptic ulcers?

A

The bacteria hide in the mucus layer and secrete agents that cause persistent inflammation that weakens to mucosal barrier. the breakdown of the mucosal barrier damages the mucosal cell layer and leaves the submucosa subject to attack by HCl and pepsin

72
Q

How does peptic ulcer treatment aim to promote healing?

A

Inhibit acid secretion
Increase muscosal resistance
Eradicate Helicobacter pylori

73
Q

What conditions are drugs that reduce acid secretion used in the treatment of?

A

Peptic ulcers
Gastro-oesophageal reflux disease
Acid hypersecretion e.g. Zollinger-Ellisonn syndrome
Cushing’s ulcers

74
Q

Give two examples of mucosal strengtheners

A

sucralfate

Bismuth chealate

75
Q

How does sucralfate work?

A

Requires an acidic environment for activation
Binds to the ulcer base and forms complex gels with mucus, providing a mucosal barrier against acid and pepsin
Increases mucosal blood flow, mucus, bicarbonate and prostaglandin production

Gastrointestinal (11 decks)

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