GI 6 Flashcards

1
Q

Three Major Salivary Glands?

A
  1. Parotid
  2. Mandibular
  3. Sublingual
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2
Q

Secretion from parotid glands?

A

watery (serous) saliva

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3
Q

Secretion from mandibular glands?

A

mixed serous and mucous

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4
Q

Secretion from sublingual glands?

A

mucous

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5
Q

Do the minor glands in the mucosa secrete mucous or serous saliva?

A

highly mucous

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6
Q

3 Functions of Saliva

A
  1. Lubrication
  2. Digestion
  3. Protection (antibacterial)
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7
Q

Is saliva in ruminants acidic or alkaline? Why?

A

Alkaline - high levels of bicarbonate and phosphate (to neutralize acid generated by fermentation)

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8
Q

Is monogastric saliva hypo-, iso-, or hyper- tonic?

A

hypotonic (very low conc. of all solutes, including sodium)

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9
Q

Hypotonic solution

A

lower concentration of solutes outside than inside the cell

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10
Q

Acinar gland

A

type of salivary gland which secretes mucus, enzymes, water, and electrolytes

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11
Q

Duct epithelium

A

absorbs electrolytes, sodium and chloride; (Secretes bicarbonate and potassium?)

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12
Q

Is ALL saliva hypotonic?

A

NO intitally it is isotonic until duct epithelium does its job

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13
Q

Why is water not absorbed by the duct epithelium?

A

cells are water impermeable

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14
Q

Is saliva secretion under any hormonal control?

A

No, it is exclusively neural (autonomic)

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15
Q

Is saliva secretion stimulated by sympathetic or parasympathetic?

A

both (mainly parasympathetic but still both)

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16
Q

What gastric secretions do parietal cells produce?

A

HCl and intrinsic factor

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17
Q

What gastric secretions do chief cells produce?

A

pepsinogen

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18
Q

What gastric secretions do surface mucous cells produce?

A

mucus and bicarbonate

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19
Q

What gastric secretion do enterochromaffin-like cells (ECL) produce?

A

histamine

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20
Q

What gastric secretions come from G cells?

A

gastrin

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21
Q

What gastric secretions come from D cells?

A

somatostatin

22
Q

What gastric “secretions” (neurotransmitters) come from nerves?

A

Ach (acetylcholine) and GRP (gastrin-releasing peptide)

23
Q

Intrinsic factor

A

produced by parietal cells and absorbs Vitamin B12

24
Q

Pepsinogen

A

inactive precursor to pepsin (enzyme) for protein digestion

25
Q

Histamine

A

paracrine from ECL cells to promote gastric acid secretion from the parietal cells

26
Q

Somatostatin

A

paracrine to inhibit gastrin secretion

27
Q

Parietal glands

A

75% of gastric glands in body of stomach, include parietal cells and chief cells

28
Q

Pyloric glands

A

in pylorus, made up of mucous cells and G cells

29
Q

Where do G cells release gastrin?

A

to the bloodstream

30
Q

Alkaline Tide

A

transient alkalization of the blood

31
Q

4 Steps of HCl Secretion from Parietal Cells

A
  1. Carbon dioxide and water undergo rxns to end upwith H+ and bicarbonate
  2. Proton pump on the lumenal/apical aspect will pump H+ out and pull K+ in
  3. Cl- follows H+ through channels (diffusion); makes HCl
  4. Bicarbonate is pumped out into blood and Cl- pulled in at the basolateral membrane
32
Q

How is alkaline tide reversed?

A

blood flows into pancreas, pancreas picks up the bicaronate and uses it to neutralize the acid in the intestine

33
Q

Size of effect of gastric acid production on blood pH?

A

Small and transient

34
Q

Is HCl secretion always stimulated by food?

A

yes

35
Q

3 Phases for HCl Secretion

A
  1. Cephalic
  2. Gastric
  3. Intestinal
36
Q

What % of HCl secretion occurs during the cephalic phase?

A

30%

37
Q

What % of HCl secretion occurs during the gastric phase?

A

60%

38
Q

Mechanisms of HCl release during Cephalic Phase

A

CNS can act directly on parietal cells with acetylcholine, or by gastrin-releasing peptde on a G cell to release gastrin which then acts via CCK2 receptor on the parietal cell

39
Q

What is different about the mechanisms of HCl release in the gastric phase?

A

includes the vagovagal reflex, involves interneurons within the enteric nervous system in addition to the same signals as the cephalic phase

40
Q

Direct Mechanism of Gastrin on HCl Secretion

A

gastrin binds to CCK2 on parietal cells to stimulate HCl secretion

41
Q

Indirect Mechnism of Gastrin on HCl Secretion

A

gastrin bind to CCK2 on ECL cells to stimulate histamine release, then histamine can act on parietal cells to stimulate HCl secretion

42
Q

Synergism of HCl Secretion

A

when gastrin (endocrine), histamine (paracrine), and Ach (NT) all act on parietal cells simultaneously

43
Q

Atropine

A

anticholinergic effect blocking the ACh binding to the M3 receptor on parietal cells

44
Q

Cimetidine

A

H2 receptor antagonist; blocks binding of histamine to parietal cells

45
Q

Omeprazole

A

proton pump inhibitor to block H+ secretion from the parietal cell into the lumen

46
Q

Somatostatin and Prostaglandin effect on HCl secretion

A

binds to its respective receptor on the parietal cell, decreases cAMP, therefore reducing activity of proton pump putting H+ into the lumen

47
Q

NSAID effect on prostaglandin

A

inhibits prostaglandin synthesis, therefore removing an inhibitory factor of acid secretion

48
Q

2 Ways Somatostatin Inhibits HCl Secretion in the Stomach

A
  1. Directly on the parietal cells
  2. Indirectly by inhibiting gastrin release

acts when stomach pH drops below 3.0ish

49
Q

Can neurons in the duodenum inhibit acid secretion by inhibiting gastrin? What about hormones?

A

no (they directly act on parietal cells)

Hormones can do both

50
Q

proenzymes

A

inactive form of an enzyme that cannot digest protein so the body doesn’t digest itself

51
Q

Zymogens

A

name for the proenzymes used in digestion

52
Q

Peptic Ulcer Disease Causes

A

mucosal loss on the protective layer, excess H+ and pepsin secretion; due to imbalance of protectiive and damaging factors in gastroduodenal mucosa