Oral & Stomach Physiology/Biochemistry - Twining Flashcards

1
Q

Give the innervation for each of the following:

  • Parotid salivary gland
  • Submandibular salivary gland
  • Sublingual salivary gland
A
  • CN IX
  • CN VII
  • CN VII
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2
Q

Give the four major constituents of gastric juice (other than water)

A
  • intrinsic factor
  • hydrogen ions
  • pepsin
  • mucus
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3
Q

Give another name for ptyalin. What does it do?

A

Also known as alpha-amylase

Starts carbohydrate digestion in the mouth

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4
Q

As new saliva travels through the ducts of the salivary gland, which ions are reabsorbed? Which are secreted?

A

Reabsorbed: Na+ (active) and Cl- (passive)

Secreted: K+ (active) and HCO3- (passive)

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5
Q

Name the major saliva component directly involved in antibacterial and antifungal defense.

Broad spectrum or narrow spectrum?

Mechanism?

A

Lysozyme

‘Narrow’ spectrum - most involved in killing gram-positive bacteria

Mechanism: cleaves beta-1-4 linkages between NAM and NAG (gram positive cell wall peptidoglycans) or NAG in fungi cell wall chitodextrins

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6
Q

Name the saliva component responsible for each of the following bacterial defenses:

  • Binds iron and prevents bacterial and some fungal growth
  • Kills bacteria by producing reactive bromide and iodine molecules
  • Secreted immunoglobulin that recognizes and binds bacteria in order to produce an immune reaction
  • Polypeptides that form pore complexes on microbial cell membranes
  • Large, highly glycosylated proteins that modulate adhesion of bacteria to oral tissues (including teeth)
A
  • Lactoferrin
  • Peroxidase
  • IgA
  • Defensins
  • Mucins
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7
Q

Saliva is low in what two ions normally found in blood plasma?

A

Na+ and Cl-

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8
Q

Desribe how the following lead to xerostomia:

  • Cystic fibrosis
  • Sjogren’s syndrome
A
  • Mutant chloride transporters lead to defective plasma secretions. Salivary mucus is thick and may clog salivary ducts, leading to xerostomia.
  • Autoantibodies to salivary gland proteins leads to the destruction of these tissues, resulting in deficient saliva production (xerostomia)
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9
Q

Name and describe the three phases of gastric secretion

A
  • Cephalic phase
    • Anticipation of food leads to vagal stimulation of the stomach, increasing production of acid and pepsin
  • Gastric phase
    • Food in the stomach excites (1) long vasovagal reflexes to/from the brain, (2) local enteric reflexes, and (3) gastrin-histamine stimulation
  • Intestinal phase
    • Presence of food in the duodenum causes small amounts of continued gastric secretion. Continued stimulation ultimately leads to inhibition of gastric secretion/emptying by an enterogastric reflex
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10
Q

Describe the substances released by the vagus nerve that influence acid secretion

A
  • ACh
    • stimulating action -> acts on parietal cells to release acid
    • stimulating action -> acts on ECL cells to release histamine
    • inhibitory action -> acts on D cells to inhibit secrtion of somatostatin
  • GRP
    • stimulating action -> acts on G cells to release gastrin
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11
Q

Describe the role of D cells in gastric secretion

A

D cells secrete somatostatin, which inhibits secretion of:

  • G cell gastrin
  • ECL cell histamine
  • Parietal cell HCl

D cells are acted upon by:

  • Stimulation - HCl from gastric parietal cells
  • Inhibition - ACh from the vagus nerve
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12
Q

Describe the role of G cells in gastric acid secretion

A

G cells release gastrin, which stimulates secretion of:

  • D cell somatostatin
  • ECL cell histamine
  • Parietal cell HCl

G cells are acted on by:

  • Stimulation - GRP from the vagus nerve
  • Inhibition - somatostatin from D cells
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13
Q

Describe the role of ECL cells in gastric acid secretion

A

ECL cells secrete histamine, which stimulates parietal cell HCl release

ECL cells are acted upon by:

  • Stimulation - ACh released from the vagus nerve
  • Inhibition - somatostatin released from D cells
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14
Q

Describe the role of parietal cells in gastric acid secretion

A

Parietal cells secrete HCl (gastric acid)

Parietal cells are acted upon by:

  • Stimulation - ACh from the vagus nerve
  • Stimulation - histamine from ECL cells
  • Stimulation - gastrin from G cells
  • Inhibition - somatostatin from D cells
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15
Q

What accounts for the observed drop in gastric [H+] after ingestion of food?

Approximately how long after ingestion of food does the rate of H+ secretion sharply increase?

A

Food buffers preexisting H+ in the stomach

H+ secretion rises sharply approximately 1 hours after food ingestion

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16
Q

Besides HCl, what else is secreted by gastric parietal cells? What is this important for?

A

Intrinsic Factor (IF)

IF is required for vitamin B12 absorption in the ileum

17
Q

Where does fat digestion begin?

What is secreted in the stomach that aids with fat digestion? What type of cell secretes it?

A

The mouth - via lingual lipase released by the salivary glands

Gastric lipase - from chief cells

Note: only about 10% of fat digestion occurs due to lingual lipase. The vast majority of fat digestion occurs in the duodenum

18
Q

What is pepsinogen?

What triggers its release?

What secretes it?

What activates it?

A

Enzyme released from gastric chief cells, responsible for protein digestion

Secretion induced by: ACH, gastrin, secretin, and cholecystokinin

Activated by HCl (or by pepsin)

19
Q

Describe the composition of mucous

A

Mucins, phopholipids, electrolytes, and water

20
Q

Appriximately how much chyme is released into the duodenum at a time?

A

a few milliliters

21
Q

Describe the general regulation of stomach emptying

A
  • self-stimulation of stomach: gastrin and stretching of the stomach wall by food stimulates increased activity of the pylorus pump
  • inhibition from duodenum: inhibits stomach contractions and increases tone of the pyloric sphincter in response to distension, mucosal irritation, acidity and osmolality of the chyme
22
Q

What part of the stomach contains ECL cells?

D cells?

G cells?

A

Corpus (body)

Antrum

Antrum