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

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Flashcards in Physiology and Pharmacology of Salivary and Gastric Secretion and Gastric Motility Deck (91)
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1
Q

What are the three pairs of salivary glands?

A

Parotid
Submandibular
Sublingual

2
Q

Where is the parotid gland located?

A

Below ear and over the masseter

3
Q

Where is the submandibular gland located?

A

Under lower edge of mandible

4
Q

Where is the sublingual gland located?

A

In floor of mouth under tongue

5
Q

What makes the saliva anti-bacterial?

A

Lysozymes, lactoferrin and immunoglobulisn

6
Q

What - in the saliva - digests complex carbohydrates?

A

Amylase

7
Q

How does the saliva neutralise acid?

A

Bicarbonate

8
Q

In the formation of saliva, what does primary secretion?

A

Acinus

9
Q

In the formation of saliva, what does secondary secretion?

A

Duct cells

10
Q

What does the formation of saliva require?

A

ATP

11
Q

What cells produce a primary secretion with Na+, K+, Cl- and HCO3- content similar to plasma, plus mucus and amylase?

A

Acinus

12
Q

What cells modify secretion by removing Na+ and Cl- and to a lesser extent adding K+ and HCO3- no movement of H2O - hence diluting?

A

Duct cells

13
Q

How much saliva a minute do we actively produce when salivating?

A

5ml

14
Q

What two things reflex regulate (neuronal control) the rate of formation of saliva?

A
  1. Simple unconditioned reflex (citrus fruits)

2. Conditioned (acquired) reflex

15
Q

In the simple (unconditioned) control of salivary secretion, what can activate pressure receptors in the mouth?

A

Food

16
Q

In the simple (unconditioned) control of salivary secretion, what happens after pressure receptors are activated by food?

A

Impulses are send via afferent nerves

17
Q

Where is the salivary centre?

A

In the medulla

18
Q

In the aquired (conditioned) control of salivary secretion, where does the signal go before reaching the salivary centre in the medulla?

A

Cerebral cortex

19
Q

What occurs as a result of the salivary centre in the medulla, sending impulses via extrnisic autonomic nerves - both paraysmpathetic and sympathetic stimulation?

A

Salivary glands increase production

20
Q

What stimulation is the dominant role in normal saliva production?

A

Parasympathetic

21
Q

What nerves does the parasympathetic stimulation control?

A

Glossopharyngeal and facial nerves

22
Q

In parasympathetic stimulation of saliva secretion, what receptors are mediated to produce large volumes of watery saliva?

A

M3 muscarinic acetylcholine receptors

23
Q

At what times is sympathetic stimulation dominant at?

A

Stressful times - dry mouth when nervous!

24
Q

In the sympathetic stimulation of saliva secretion, what do postganglionic fibres from superior cervical ganglia cause?

A

Small volume, thick, mucus rich saliva, mediated by B1-adrenoceptors

25
Q

How much capacity does the stomach have?

A

50 > 1000ml

26
Q

What nerve causes relaxation of the stomach to accomodate food from the oesophagus?

A

Vagus

27
Q

What two acids are secreted in the stomach, for the start of protein digestion?

A

Pepsin and hydrochloric acid

28
Q

Where does the stomach secrete gastric juice from?

A

Gastric pits in the gastric mucosa

29
Q

What wave strength determines the escape of chyme through the pyloric sphincter?

A

Antral ave

30
Q

What do gastric factors and duodenal factors govern?

A

Antral wave

31
Q

What does distention of the stomach increase?

A

Motility, due to stretch of smooth muscles

32
Q

When smooth muscles of the stomach are stretched, what is stimulated, increased and released?

A

Intrinisc nerve plexuses, increased vagus nerve activity and gastrin release

33
Q

What reflex can delay empyting of the stomach?

A

Enterogastric reflex

34
Q

What does the enterogastric reflex do by signals from the intrinisc nerve plexus and autonomic nervous sytem?

A

Decrease antral peristalic activity

35
Q

Name two enterogastrones?

A

Secretin and cholecystokinin (CKK)

36
Q

What do release of enterogastrones from the duodenum inhibit?

A

Stomach contraction

37
Q

What food substance has an imporant role in delaying gastric emptying required for digestion and absorption in small intestine?

A

Fat

38
Q

What does acid in the duodenum do to stomach contractions?

A

Slows it to allow time for neutralisation by bicarbonate from pancreas

39
Q

What are two main areas of the stomach, important in secretions?

A
Pyloric gland area (PGA)
Oxyntic mucosa (OM)
40
Q

What do D cells secrete?

A

Somatostatin

41
Q

What do G cells secrete?

A

Gastrin

42
Q

Where are D cells and G cells located?

A

In the pyloric gland area

43
Q

What do chief cells secrete?

A

Pepsinogen

44
Q

What do Enterochromaffin cells release?

A

Histamine

45
Q

What do parietal cells secrete?

A

Hydrochloric acid and intrinsic factor

46
Q

Where are parietal cells, enterochromaffin like cells and chief cells found?

A

In the oxyntic mucosa (OM)

47
Q

What does gastrin stimulate?

A

HCl secretion

48
Q

What does somatostatin inhibit?

A

HCl secretion

49
Q

What are three functions of HCl released from parietal cells?

A
  1. Activates pepsinogen to pepsin
  2. Denatures protein
  3. Kills micro-organisms ingested with food
50
Q

What does pepsinogen released from chief cells do?

A

Inactive precursor of the peptidase, pepsin

51
Q

What does intrinsic factor released from parietal cells do?

A

Binds vitamin B12, allowing absorption in the terminal ileum

52
Q

What 4 receptors does the parietal cell have?

A
  1. Muscarinic ACH receptor 3
  2. Gastrin (CCK2) receptor
  3. Histamine receptor
  4. Prostaglandin receptor
53
Q

Where does cholinergic nerve (postganglionic parasympathetic) meet, and what does this cause?

A

Meets M3 receptor on parietal cell, causing HCl release

54
Q

What happens once gastrin has landed on an enterochromaffin like cell?

A

Cell releases histamine which acts on H2 receptors on parietal cell to release HCl

55
Q

What two receptors are present on an enterochromaffin cell?

A

Gastrin CCK2 receptor

M1 ACh receptor

56
Q

What does enterochromaffin cell release to cause HCl secretion?

A

Histamine

57
Q

What inhibits gastrin between meals?

A

Somatostatin

58
Q

What does activation of the PGE receptor on parietal cells do?

A

Inhibits all stimulating signals, and prevents HCl secretion

59
Q

During the resting state of the parietal cell, what can be said about the H+/K+ATPase?

A

It is largely within the cytoplasmic tubulovesicles

60
Q

What occurs to the H+/k+ATPase when the parietal cell is stimulated?

A

Traffics to the apical membrane taking residence in extended microvilli

61
Q

What phase of gastric secretion occurs before food reaches stomach?

A

Cephalic

62
Q

What phase of gastric secretion occurs when food is in the stomach?

A

Gastric

63
Q

What phase of gastric secretion occurs when food has left the stomach?

A

Intestinal

64
Q

What nerve is activated when smell and taste of food occurs?

A

Vagal activation

65
Q

The vagal activation stimulates an enteric neurone to do what?

A

Increase ACh

66
Q

What does ACh do to a D cell, and what does it do to ECL cell?

A

Inhibits D cell

Stimulates ECL cell

67
Q

Other than ACh what else does enteric neurone increase?

A

Increases GRP (gastrin releasing peptide)

68
Q

What does the GRP from enteric neurone, during eating stimulate?

A

G cells to secrete gastrin etc

69
Q

What two factors in the gastric phase. cause increased secretion, and what do they act on to achieve this?

A

Distension - enteric neurone

Protein digestion products - G-cell

70
Q

What does a low pH in the stomach, drive secretion of?

A

Somatostatin

71
Q

What class of drugs block competitevly and an example of one is pirenzepine?

A

Muscarinic receptor antagonists

72
Q

What class of drugs (ranitidine) block competitively the H2 receptor on parietal cells?

A

H2 receptor antagonistst

73
Q

What drugs block cyclo-oxygenase (which stimulates prostaglandin receptor on parietal cells), and so increase acid secretion?

A

NSAIDs block irreversibly

74
Q

What drugs (omeprazole) block by covalent modification at the H+K+ATPase?

A

PPIs

75
Q

What three effects does locally produced prostaglandins (PGE and PGI) have in relation to protection of the mucosa from attack by HCl and pepsin?

A
  1. Reduce acid secretion
  2. Increase mucus and bicarbonate secretion
  3. Increase mucosal blood flow
76
Q

What term is given to ulcers in an area where the mucosa is exposed to hydrochloric acid and pepsin (stomach/duodenum)?

A

Peptic ulcers

77
Q

What reduces prostaglandin formation (COX 1 inhibition)?

A

NSAIDS

78
Q

What can gastric damage due to long-term NSAID treatment be prevented with?

A

PGE analogue (misoprostol)

79
Q

Name a drug that inhibits basal and food stimulated gastric acid formation and maintains secretion and mucus and bicarbonate?

A

Misoprostol (stable PGE analogue)

80
Q

What, protected in teh mucus gel, secretes agents causing a persistent inflammation that weakens the mucosal barrier?

A

H.pylori

81
Q

Name a syndome that involves a rare, gastrin producing tumour?

A

Zollinger-Ellison syndrome

82
Q

What condition causes heightened vagal tone, leading to acid hypersecretion?

A

Cushing’s ulcer

83
Q

What drugs inhibit the membrane inserted (micro villi) H+/K+dependent ATPase (proton pump)?

A

PPIs

84
Q

What sort of proton pumps are not inhibited by PPIs?

A

Ones in the tubulovesicles

85
Q

What kind of drugs are PPIs, because they are inactive at neutral pH (proton pump hidden in tubulovesicles)?

A

Prodrugs

86
Q

Where are absorbed PPIs delivered to?

A

The secretory canaliculi of the stomach

87
Q

When PPIs are in the secretory canalicula of the stomach, what are they activated to?

A

Sulfenamide (then block lumenal sulphydrl groups of membrane inserted proton pump)

88
Q

What is a complex of aluminium hydroxide and sulphated sucrose?

A

Sucralfate

89
Q

Name two mucosal strengtheners?

A

Sucralfate

Bismuth chealate

90
Q

What does sucralfate release to acquire a strong negative charge?

A

Aluminium

91
Q

What is used in combination with antibiotics, H2 receptor antagonists ro promote eradication of H.pylori?

A

Bismuth chealate