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NME > Salivary and Gastric Secretions > Flashcards

Salivary and Gastric Secretions Flashcards

1
Q

Exocrine Glands

A
  • with duct
  • salivary glands, gastric glands
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2
Q

Endocrine Glands

A
  • without duct
  • enteroendocrine cells in the
    stomach and small intestine
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3
Q

Role of Salivary Secretions

A
  • lubrication
  • protection; oral hygiene/
    antimicrobial agents
  • initiate chemical digestion
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4
Q

Major Salivary Glands (3):

A
  • parotid
  • submandibular
  • sublingual
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5
Q

Dispersed Salivary Glands:

A
  • mucosa of mouth and tongue
  • labial, buccal, palatal, lingual
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6
Q

Hypotonic:

A

solution has a lower concentration
of solutes and a higher
concentration of water than inside
the cell [water moves into cell

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7
Q

Hypertonic:

A

solution has a higher concentration of solutes and a lower concentration of water than inside the cell [water moves out of cell]

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8
Q

Major Salivary Glands

A
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9
Q

Parotid Gland Secretions: proportions and description:

A
  • 25%
  • serous, watery secretions
    containing salivary amylase for
    starch digestion
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10
Q

Submandibular Gland Secretions: proportion and description:

A
  • 70%
  • mixed serous and mucus
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11
Q

Sublingual Gland Secretions: proportion and description:

A
  • 5%
  • Mucus: thicker mucus dominant
    secretions for lubrication
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12
Q

Saliva Composition and Functions:

A
  • alpha not a
  • disaacharide and trisaccharide
    important
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13
Q

Saliva Composition and Functions:

A

insert table

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14
Q

Acinar Structure of Salivary Glands:

A
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15
Q

Two Stage Formation of Hypotonic Saliva:

A

Cl- goes inside cell and into ductal area
Na+ enters via ductal area
Active transport in ductal area: Na+ out, K+ in
and Na+ and HCO3- out
hence at end stage of saliva hypotonic

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16
Q

Composition of Saliva changes with flow rate: Low rate of secretion:

A

max reabsorption of electrolytes produces hypotonic saliva (lower conc of osmotically active electrolytes)
more K+++

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17
Q

Composition of Saliva changes with flow rate: High rate of secretion:

A

reduced reabsorption of electrolytes produces saliva with higher osmolality closer to primary isotonic solution produced by acini
more sodium due to less absoprtion time ***
low secretion…

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18
Q

Electrolytes in saliva hypotonic: Na+. Cl-, HCO3-, K+

A

Na+ and Cl- < plasma
HCO3- and K+ > plasma

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19
Q

Composition of Saliva changes with flow rate:

A
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20
Q

ANS control of Salivary Secretion Rate: Parasympathetic stimulation:

A

Sensory stimuli pertaining to foodstuff stimulates salivary nuclei in the brainstem via CN VII (7) [facial nerve > sublingual and submandibular] and CN IX (9)[glossopharyngeal nerve> parotid].

This results in an increase in amylase, mucin, and serous saliva; also vasodilation

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21
Q

ANS control of Salivary Secretion Rate: Sympathetic stimulation:

A

Facilitated via superior cervical ganglion and sympathetic postganglionic nerves, leading to vasoconstriction and reduced saliva production.

A dry mouth by be reported???

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22
Q

ANS control of Salivary Secretion Rate:

A
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23
Q

Sjögren’s syndrome:

A

Autoimmune disease that destroys the exocrine glands which commonly affects tear and saliva production resulting in dry eyes and a dry mouth. These are collectively known as sicca symptoms [derived from the Latin, siccus, meaning dry].

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24
Q

Xerostomia [dry mouth]

A

Patients lack adequate saliva, tooth decay and halitosis (foul smell) is common due to bacterial overgrowth. There may also be difficulty speaking or swallowing solid food due to inadequate lubrication.

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25
Q

What is Schirmer’s test used for?

A

Employed to determine if an individual produces enough tears to keep their eye moist and healthy.

Used to assess for problems of dry eyes [including Sjögren’s syndrome].

26
Q
A

Schirmer’s test

27
Q

How is Schirmer’s test conducted?

A

Litmus paper folded and placed in cells

Will show dryness

Filter paper in situ for 5 mins, before assessing the result.

28
Q

What branches into gastric glands?

A

Gastric pits in the mucosa, branch into gastric glands

29
Q

Exocrine Gland Cells (3):

A

Mucous neck cells – thin mucus
Parietal cells - HCl and intrinsic factor
Chief cells – pepsinogen, gastric lipase

30
Q

Secretions

A

insert diagram (numbers not needed)

31
Q

Endocrine Gland Cells:

A

G cells - hormone gastrin
D cell hormone somatostatin [GHIH]
Enterochromaffin-like [ECL] cells secrete histamine

32
Q

Gastric Glands

A
33
Q

Gastric Stimulation: Parasympathetic :

A
  • Vagus Nerve: distension, peptide
  • Parietal cell secretion of HCl
  • Chief cell secretion of pepsinogen
  • Lower oesophageal sphincter
    contraction
  • Increases motility of stomach
  • Relaxes pyloric sphincter
34
Q

Gastric Secretion Promotes Gastric Digestion:

A
35
Q

Gastric Juice Components:

A
  • water and electrolytes
  • mucus (glycoprotein mucin)
  • pepsinogen pro-enzyme, gastric
    lipase, rennin (chymosin)
  • HCL (pH 1-3)
  • Intrinsic Factor (IF)
    WEPLRHCLIF
36
Q

Gastric Juice Components:

A
37
Q

HCl secretion by parietal cells

A
38
Q

What stimulates gastric acid secretion?

A

Ach released from vagus Gastrin from G cells
Histamine from ECL cells

39
Q

Secretory IgA and serous IgA difference

A

pentameric (secretary)???
monomaric (serous)

40
Q

Inhibition of Gastric Acid Secretion:

A
  • Stomatostatin from D cells
    (paracrine* and endocrine): inhibits
    adenylate cyclase
  • Mucosal Prostaglandin anatagonist
    for H2 receptor: NSAIDS inhibit
    prostaglandin formation and
    increase gastric acid secretion
41
Q

Sympathetic activity in salivary glands result in patient complaining of

A

dry mouth

42
Q

Signaling between neighbouring molecules is

A

paracrine

43
Q

parietal cells adaptations for acid secretion:

A
  • parietal cells are packed with
    tubulovescicles in resting state
  • on stimulation these fuse with the
    canalicular membrane as microvilli
  • contain H+/K+ ATPase and carbonic
    anhydrase enzymes needed for
    production and secretion of H+
44
Q

Proton Pump Inhibitor: Example and function

A
  • omneprazole (core drug)
  • inactivates K+/K+ ATPase
45
Q

Pharmacological inhibition of gastric acid (3):

A
  • Proton Pump Inhibitor
  • H2 receptor antagonist
  • Atropine
46
Q

H2 receptor antagonist: example and function:

A
  • cimetidine
  • inhibits stimulus for acid secretion
47
Q

Atropine function (gastric acid)

A
  • inhibits muscarinic receptors and vagal stimulation of acid secretion
48
Q

Which cells secrete HCl?

A
  • parietal cells
49
Q

State the names of the three phases of gastric secretion:

A
  • cephalic
  • gastric
  • intestinal
50
Q

Description of three phases of gastric secretion:

A
  • Cephlaic: vagus innervates parietal,
    chief and gastrin secretion
  • Gastric: stimulation fo parietal,
    chief, mucus secretion, G cells
  • Intestinal:
    Excitatory: chyme with pH >3,
    peptides stimulate gastric
    secretions via vagus and gastrin
       Inhibitory: Chyme with pH: 
   chyme with pH<2, protein 
   breakdown products, changes 
   in osmolarity larger, inhibits 
   gastric secretions via 
  cholecystokinin, gastric 
  inhibitory polypeptide
51
Q

Three phases of Gastric Secretion:

A
52
Q

Cephalic Phase Overview:

A
  • get started phase

The taste, smell, or thought of food stimulate the vagal centre [medulla oblongata]. Vagal signals are sent to endocrine cells within the GI system. This results in the secretion of gastrin.

53
Q

Gastric Phase Overview:

A
  • go for it phase

Distention of the stomach occurs, preparing for entry of bolus. The greatest volume of gastric juice is produced during this phase.

54
Q

Intestinal Phase Overview:

A
  • slow down phase

This phase can promote or inhibit the further production of gastric juices as well as controlling rate at which stomach contents can enter the duodenum.

55
Q

Why is gastric mucosa not damaged?

A
  • surface mucous glands secrete
    viscous mucus layer generating a
    mucosal barrier
  • mucin has basic side chains which
    prevent the neutralisation of mucin
    and HCO3 is secreted from surface
    epithelial cells - both mechanisms
    nuetralise H+ ions
  • tight junctions stop acid damaging
    underlying tissue

Net result - unstirred layer is pH7, pepsinogen not activated, prevents damage

56
Q

Gastritis:
- is
- caused by (most commonly)
- other causes
- recovery

A
  • inflammation of the gastric mucosa
  • most commonly caused by an
    infection by the bacteria
    Heliobacter Pylori (50% of pop
    have)
  • smoking, alcohol, NSAIDs, etc
  • following acute damage, rapid
    regeneration is via a process called
    restitution - rapid division of stem
    cells located in the neck of gastric
    glands
57
Q

Restitiution

A

rapid division of stem cells located in the neck of gastric glands

58
Q

Which is a major salivary gland?

  • lacrimal gland
  • sweat gland
  • parotid gland
  • sebaceous gland i
A

parotid gland

59
Q

Which ion is present in the highest concentration in hypotonic saliva?

  • Cl-
  • Mg
  • K+
  • Na+
A

Potassium

60
Q

Which exocrine gland cell secretes HCl in the stomach?

  • mucous neck cells
  • chief cells
  • parietal cells
  • G cells
A

parietal cells

61
Q

A 50 year old woman presents to the GP with complaint of indigestion and heartburn. GP prescribed omneprazole. What is the mechanism of action?

  • blocked chief cells of gut
  • activate H+/Cl- ATPase pump
  • activate H+/K+ ATPase pump
  • blocked H+/K+ ATPase pump
A
  • activate H+/Cl- ATPase pump
62
Q

In one of the gastric secretion phases, the tase of food stimulates the vagal centre which then activates the gut cells to secret gastrin. Which phase?

  • gastric phase
  • intestinal phase
  • cephalic phase
  • oesophageal phase
A

cephalic phase

NME (52 decks)

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