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module 104 - theme 1 > salivary & gastric secretions > Flashcards

salivary & gastric secretions Flashcards

1
Q

what are exocrine glands?

A

glads with a duct

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2
Q

what are endocrine glands?

A

glands without a duct

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3
Q

give some examples of exocrine glands

A
  • salivary glands

- gastric glands

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4
Q

give some examples of endocrine glands

A

enteroendocrine cells in stomach and small intestine

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5
Q

what is the role of salivary secretions?

A
  • lubrications
  • protection (oral hygiene)
  • imitate chemical digestion
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6
Q

what are the 3 main salivary glands?

A
  • parotid
  • submandibular
  • sublingual
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7
Q

where are the salivary glands dispersed?

A
  • mucosa of mouth and tongue

- labial, buccal, palatal, lingual

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8
Q

what are the key features of parotid glands?

A
  • serous

- watery secretions containing salivary amylase for starch digestion

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9
Q

what are the key features of submandibular glands?

A

mixed serous and mucus

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10
Q

what are the key features of sublingual glands?

A

mucus: thicker mucus dominant secretions for lubrications

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11
Q

what are the unique properties of acinar structure of salivary glands?

A
  • large volume of saliva produced compared to gland
  • low osmolarity
  • high potassium concentrations
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12
Q

what are the 2 stages of hypotonic saliva formation?

A

1) acinar cells secrete isotonic saliva similar to blood plasma in electrolyte composition
2) ductal cells secrete HCO3- and K+ ions with reabsorption of NaCl and limited movement of water by osmosis. This produces HCO3- and K+ rich hypotonic saliva

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13
Q

how does the composition of saliva change with low rate of secretion?

A

maximum reabsorption of electrolytes produces hypotonic saliva

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14
Q

how does the composition of saliva change with the high rate of secretion?

A

reduced reabsorption of electrolytes produce alkaline, HCO3- rich saliva with increased osmolarity closer to that of primary isotonic saliva

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15
Q

how does the parasympathetic ANS regulation dominate the salivary & gastric secretions?

A
  • sight, thought, smell, taste, tactile stimuli, nausea
  • signal superior and inferior salivary nuclei in the medulla
  • via cranial nerve VII (facial nerve) for the sublingual and submandibular gland
  • cranial nerve IX (glossopharyngeal nerve) for the parotid gland
  • increase salivary secretion, vasodilation, myoepithetlail cell contraction
  • inhibitors: fatigue, sleep, fear, dehydration
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16
Q

how does the sympathetic system stimuli neural system?

A
  • overall slight increase in secretion
  • produces mucin and enzyme rich saliva
  • activity is via superior cervical ganglion
  • initial vasoconstriction
  • later vasodilation
17
Q

what is Sjogren’s syndrome?

A
  • salivary gland dysfunciton
  • an autoimmune disease that destroys the exocrine glands
  • commonly affects tear and salivary production
  • dry eyes and dry mouth, known as sick symptoms
18
Q

what is Xerostomia?

A
  • salivary gland dysfunction
  • dry mouth
  • patients lack inadequate saliva
  • dental caries and halitosis common due to bacterial overgrowth
  • difficulty speaking or swallowing solid food due to inadequate lubrication
19
Q

what are the 2 types of gastric glands?

A
  • body & fundus

- antrum

20
Q

what are the key features of body & fundus gastric glands?

A
  • 80%
  • gastric/oxyntic glands
  • exocrine secretion of HCl, pepsinogen, intrinsic factor and mucus
  • paracrine ECL cell secretion of histamine, paracrine D cell secretion of somatostatin
21
Q

what are the key features of antrum gastric glands?

A
  • 20%
  • pyloric glands
  • mucus and endocrine hormone gastrin
  • paracrine/endocrine somatostatin
22
Q

how is HCl secreted by parietal cells?

A
  • parietal cells have an intracellular branched canalicular structure and are packet with tubulovesicles in resting state
  • these contain enzymes carbonic anhydrase and H+/K+-ATPase for acid secretion
  • on stimulation of acid production tubulovesicles fuse with the canalicular membrane to form microvilli
  • HCl is formed at these microvilli and secreted
23
Q

how does HCl secretion occur?

A
  • H+/K+-ATPase proton pump drives active secretion of H+
  • carbonic anhydrase (CA) catalysed formation of HCO3- producing H+ ions
  • HCO3- exchanged for Cl-
  • Cl- diffuses into lumen
24
Q

what activates gastric acid secretion?

A
  • ACh: acetylcholine release from vagus
  • gastrin: from G cells
  • histamine: from ECL cells
25
Q

what inhibits gastric acid secretion?

A
  • somatostatin: from D cells which inhibits adenylate cyclase (AC)
  • mucosal prostaglandin antagonists for H receptor
26
Q

what are the pharmacological inhibitors of gastric acid?

A
  • omeprazole: proton pump inhibitor inactivates H+/K+-ATPase
  • cimetidine: H2 receptor antagonist inhibits stimuli for acid secretion
  • atropine: inhibits muscarinic receptors and vagal stimulation of acid secretion
27
Q

what are the 3 phases of gastric secretion?

A
  • cephalic
  • gastric
  • intestinal
28
Q

what happens in the cephalic phase of gastric secretion?

A

vagus stimulated parietal, chief cell production of gastric juice and hormone gastrin secretion

29
Q

what happens in the gastric phase of gastric secretion?

A

stimulate parietal, chief mucus secretion, antral G cells

30
Q

what happens in the intestinal phase of gastric secretion?

A
  • excitatory: chyme with pH>3, peptides stimulate gastric secretions via vagus and gastrin
  • inhibitory: chyme with pH<2, distention, protein breakdown produces hypo/hyper-osmotic products, inhibit gastric secretions via cholecystokinin, secretion, gastric inhibitory polypeptide
31
Q

why is the gastric mucosa not damaged?

A
  • surface mucous glands secrete viscous mucus layer of mucopolysaccharides/proteins
  • mucus viscosity generates mucosal barrier: mucin has basic side chains. HCO3- secreted from surface epithelial cells. Both neutralise H+ ions
  • tight junctions stop acid damaging underlying tissue
  • net result: unstirred layer is around pH7, pepsinogen not activated, prevents enzymatic and chemical damage
32
Q

what are the key features of gastritis?

A
  • dysfunction & inflammation of gastric mucosa
  • most commonly caused by an infection by the bacterial Helicobacter pylori
  • gram negative bacteria produce urease which forms ammonia from urea, ammonia neutralises bacterial acid and is toxic to mucosal barrier
  • also caused by smoking, alcohol, non-steroidal anti-inflammatory drugs, chronic stress
  • following acute damage, rapid regeneration is via a process caused restitution: rapid division of stem cells located in neck of gastric glands
33
Q

what is autoimmune atrophic gastritis?

A
  • an antibody mediated destruction of gastric parietal cells, which causes hypochlorydria and a deficiency of intrinsic factor If
  • the loss of If results in vitamin B12 Mal-absorption and pernicious anaemia

module 104 - theme 1 (17 decks)

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