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Oral Sciences > Unit 2 > Flashcards

Unit 2 Flashcards

1
Q

SG’s are these types of glands:

A

exocrine, merocrine, compound (numerous acini)

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2
Q

Parenchyma of the sg’s:

A

acini

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3
Q

6 stages of SG development:

A

BEBLLD: bud, epi cord, branching, lobule, lumen, differentiation

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4
Q

initiates sg formation:

A

thickening of oral epi

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5
Q

What is the inital bud surrounded by after evagination?

A

condensed mesenchyme that has an endo plexus (6-8wks)

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6
Q

Shape of oral epi cells that form initial bud:

A

hexagonal

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7
Q

TF? Growth of initial bud stops with development of the epi cord.

A

F. continued growth of epi cord

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8
Q

When does the epi of the epi cord become innervated?

A

onset of development

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9
Q

These form the PSG:

A

neural crest-derived neurons, come together at primary duct

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10
Q

Branching is successive rounds of:

A

end bud clefitng, epi proliferation, secondary duct formation

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11
Q

Signals involved in branching:

A

fibronectin (from mesenchyme), FGF-10, signals from PSG

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12
Q

Lobules are formed from:

A

CT

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13
Q

functional unit of salivary gland:

A

acinus

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14
Q

Responsible for formation of duct lumen:

A

VIP

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15
Q

Source of VIP

A

PSG

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16
Q

Stages of lumenal development:

A

Proliferation, Condensation, polarization, lumen formation, lumen expasion

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17
Q

drives expansion of the lumen:

A

fluid movement through vessel

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18
Q

Cell lining lumen:

A

K19+ luminal cell

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19
Q

of cell types that make up terminal bulb

A
  1. MAD: myoepi, acinar, and ductal
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20
Q

Structures derived from terminal buds:

A

intercalated duct, myoepi cells, acinar cells

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21
Q

These become acinar cells:

A

proacinar cells

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22
Q

Protein involved in epi-mesenchyme reactions:

A

integrin

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23
Q

Steps in gland/ innervation development:

A

Initiation, gangliogenesis, innervation of branching epi, lumenization

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24
Q

Involved in the proliferation of initial bud and duct cells:

A

FGF-10

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25
Q

involved in acinus/ branching morphogenesis

A

epi-mes interactions (I SEcrete: intercalated, striated, excretory)

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26
Q

Mucus cells are filled w:

A

mucus granules

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27
Q

Serous cells distal or proximal to mucous acini?

A

distal

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28
Q

Closer to the intercalated ducts, serous or mucous cells?

A

mucous

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29
Q

Serous cells are connected to lumen via:

A

secretory (intercellular) canaliculi, bw mucous cells

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30
Q

Location of myoepi cells:

A

bw basolamina and acinar or duct cells (extend to intercalated ducts)

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31
Q

Tissue origin of myoepi cells:

A

ectoderm, oral epi

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32
Q

How to id intercalated duct cells:

A

low cuboidal, central nucleus, few organelles ,secretory granules

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33
Q

How to id striated duct cells:

A

columnar, central nucleus, basal striations-mito in parallel, small secretory grnaules

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34
Q

Assoc w small secretory granules of striated duct cells:

A

EGF, fibronectin, kallikrein

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35
Q

Lumen of striated duct cells, permeable to water?

A

no

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36
Q

Function of mito in striated duct cells:

A

active transport/ reabsorption of Na+

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37
Q

Na+ enters here after reabsorption in striated duct cells:

A

duct cells and CT

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38
Q

How to id prximal excretroy duct:

A

simple or pseudostratified epi, basal cells bw columnar, some w lipofuscin granules, amorphous saliva in center

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39
Q

How to id distal segment of excretory duct:

A

stratified columnar epi, goblet cells, amorphous saliva in center

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40
Q

Relative contributions of major Sg’s:

A

SM: 60%, P: 25%, SL:7%, minor: 7%

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41
Q

SMg opens here:

A

either side of frenulum of tongue

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42
Q

SLg opens here:

A

near SMg opening, ducts of Rivinus

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43
Q

Striated ducts of the major SG’s:

A

P and SM: prominent, SL: Short

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44
Q

Intercalated ducts of the major Sg’s:

A

P: Long, SM: shorter, SL: absent

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45
Q

Relative mucus/ serous contribution of SMg:

A

more serous than mucus

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46
Q

Minor sg’s are not found here:

A

gingiva, vent tongue, central hard palate (sg tumors will not be found in these spots)

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47
Q

Location of minor sg’s:

A

SUBmucosa, loose CT

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48
Q

TF? All minor sg’s are mucus.

A

F. all except von Ebner’s (pos tongue)

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49
Q

Ducts of minor sg’s:

A

short

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50
Q

% contribution of minor sg’s to total mucus secretions:

A

70%

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51
Q

TF? Minor sg’s play a role in mucosal immunity.

A

T

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52
Q

Sg’s that are only serous:

A

von Ebner and P

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53
Q

intercellular juncitons of acinar cells:

A

Tight junc, adherens junc, and desmosomes

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54
Q

Proteins assoc with tight junctions:

A

occludins, claudins

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55
Q

Proteins assoc with adherens junctions:

A

E-cadherin, catenin, p120, connected with actin

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56
Q

Proteins assoc with desmosomes:

A

desmoglein, desmoplakin, plakoglobin, connected with keratin

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57
Q

Which region of the intercellular junction is the the apical portion found in?

A

lateral (NOT baso-lateral!)

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58
Q

Fxns of tight jun, adh jun, and desmosomes:

A

permeability barrier, cell shape, stability

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59
Q

p120 knockout mice get:

A

duct cell tumors

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60
Q

3 factors in sg secretion:

A

gustatory stimulation, chewing, neuronal control

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61
Q

Para to SM/SL glands:

A

sup s. nuc. (brainstem), glossopalatine nerve, geniculate gang, chorda tympani n. (CNVII), lingual n., subm gang, glands

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62
Q

Para to P gland:

A

inf sal nuc (brainstem), CNIX, jugular gang, tympanic n., otic gang, p gland

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63
Q

Sym to glands:

A

T1 and T2 (thoracolumbar region), sup cervical gang, (middle meningeal a. to otic gang, to P) OR (maxilary a. to subm gang, to glands)

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64
Q

2 groups of nerve endings to acinar cells:

A

bw acinar cells and next to BL, all unmy

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65
Q

dictates the type of saliva produced:

A

neurotransmitter

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66
Q

Receps for sym and para nerves:

A

S: a/beta adrenergic. P: cholinergic

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67
Q

NT that leads to protein rich secretions, nt that leads to watery saliva:

A

NE, AcH

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68
Q

signal to help maintain branching:

A

neuturin, given after radiation

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69
Q

Leads to reduced expression of neuturin, and results of the reduced expression:

A

Apoptosis because of diminished para fxn, reduced neuturin leads to increases neuronal apoptosis

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70
Q

Tx with neutrurin:

A

red neuronal apoptosis, restores para fxn, inc epi regeneration

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71
Q

Leads to red para innervation:

A

HaN radiaiton

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72
Q

Gross comp of saliva:

A

99% water, 0.5% inorganic, 0.5% organic (crevicular fluid, bacteria, food, cellular debris, epi cells, pmns)

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73
Q

Crevicular fluid is:

A

serum exudate

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74
Q

of oral bac:

A

100 million (10^8)

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75
Q

Watery to viscous of the sg’s:

A

P, SM, then SL

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76
Q

pH of saliva:

A

6.7 (5.6 - 8.0) 5.5 is the critical point for caries formation

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77
Q

of swallows per day and amt of bac swallowed each day’

A

2,500, 1-2.5g

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78
Q

__ml swallowed with each swallow:

A

0.3ml

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79
Q

Minor sg’s:

A

labial, palatal, lingual (von Ebners), buccal

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80
Q

Resting contribution to total saliva:

A

SM/SL: 70%, P: 20%, Minor: 10%

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81
Q

Stimulated contribution to total saliva:

A

SM: 35%, P: 50%, SL: 7%, SM: 7%

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82
Q

Influence salivary flow:

A

body position, chemical stimulation, irritation of esophagus/ stomach

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83
Q

Gallons of saliva produced in a lifetime:

A

10,000

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84
Q

kg of protein produced in a lifetime:

A

190kg

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85
Q

Digestive function of saliva in regards to commensal microbes:

A

colonization, adhesion, nutrient

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86
Q

Proteective function of saliva in regards to pathogens:

A

Clearance, agglutination, Killing

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87
Q

Fxns of saliva:

A

water balance, excretion, antimicrobial, remineralization, form enamel pellicle, produce biological active substance

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88
Q

subtratum for bacterial adhesion

A

enamel pellicle (proteins adsorption to tooth surface)

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89
Q

Inorganic components of saliva:

A

CaPO4, KCl, NaHCO3, F, SCN, MgSO4, I, CO2, N2, O

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90
Q

Increased conc’s of Ca and PO4 can lead to:

A

mineralized plaque/ tartar

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91
Q

Low mol w8 organic components:

A

urea, uric acid, free amino acids, lipids, creatinin, ammonia, glucose, cAMP, corticosteroids

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92
Q

Intrinsic proteins:

A

derived from acinar cells

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93
Q

List intrinisic proteins:

A

Sal amylase, Acidic PRP, Basic PRP, proline-rich glycoprotin, cistatin, histatin, mucins, peptides, statherin

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94
Q

Fxn in remineralization:

A

Cistatin, histamine, statherin,

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95
Q

Gs that release acidic PRP’s:

A

P and SM

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96
Q

Highest to lowest composition of intrinsic proteins:

A

amylase, PRP, prloline-rich glycoprotein, statherin/cistatin, mucins

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97
Q

Extrinsic proteins in saliva:

A

sIgA, Lysozyme, lactoperoxidase, lactoferrin, cytokines, albumin, IgG, IgM, lipoproteins, serumproteins, and enzymes

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98
Q

how does sIgA enter the sg’s?

A

via lymphocytes in surroundings in acini, taken into acinar cell

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99
Q

indicator of contribution of serum exudate to whole mouth saliva:

A

serum albumin

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100
Q

Fxns of mucins:

A

digestion, lubrication, tissue coating, anti-viral/ bacterial

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101
Q

Fxns of histatins:

A

anti-fungal/ bacterial, buffering, mineralization

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102
Q

Fxns of cystatins:

A

anti-viral, mineralization, tissue coating

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103
Q

Fxn of statherin:

A

tissue coating, lubrication, mineralization

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104
Q

Fxns of PRP:

A

mineralization, tissue coating

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105
Q

Fxn of amylases:

A

digestion, tissue coating, antibacterial

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106
Q

Antibacterial fxns:

A

CHAMP: cystatin, histatins, amylases, mucins, peroxidases

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107
Q

Anti-viral fxn:

A

Cystatins, mucins

108
Q

Anti-fungal:

A

histatin

109
Q

Tissue coating:

A

CAMPS: cystatins, amylases, mucins, PRP, statherins

110
Q

Fxn in lubrincation:

A

mucins, statherin

111
Q

Fxn in mineralization:

A

CHPS: cystatins, histatins, PRP, statherins

112
Q

Fxn in digestion:

A

amylases, mucins

113
Q

Fxn in buffering:

A

carbonic anhydrase, histatins

114
Q

Most abundant protein in saliva:

A

amylase

115
Q

Amylase breaks:

A

alpha 1-4 lycosidic bonds

116
Q

pH range of amylase:

A

3.8-9.2 (stomach 3.5)

117
Q

TF? Salivary amylase in functional in the stomach.

A

F

118
Q

How do isoenzymes of salivary amylase differ?

A

glycosylation

119
Q

MG1 is aka:

A

muc5b

120
Q

Mucins:

A

high mol. w8, high CHO (carb side chains/glycans), sulfate groups, hard and soft tissue, enamel pellicle, bacterial adhesion (colonization), bacterial aggregation (clearance), blood group antigens (secretors), lubricant

121
Q

Structure of MG1:

A

over 1000kD, multiple subunits, about 85% CHO, complex oligosaccharides (ABH, Lea, Leb blood group antigens)

122
Q

Structure of MG2:

A

200-250 kD, single apomucin, about 70% CHO, O-glycosidic linkages

123
Q

This mucin is evolutionarily younger:

A

MG2, only in mammalian lineage

124
Q

Responsible for mucous lubrication:

A

negative charge on glycans

125
Q

Salivary agglutination is aka:

A

gp-340

126
Q

gp-340:

A

in pellicle, adhesion and aggregation of S. mutans, same as lung glycoprotein, spliced from DMBT1, TSG, member of scavenger receptor cysteine-rich superfamily (SRCS), 45% carb - 6% sialic acid (a2,3 linked), 12 fucose (a1,2 linked), innate response, made by sgs

127
Q

Blood group and Lewis-antigens depend on:

A

secretor status

128
Q

Basic PRP’sL

A

bind membranes, protect against tannins

129
Q

Acidic PRP’s:

A

Ca2+ binding proteins, , remineralization, bacterial adhesion counter receptors

130
Q

Proline-rich glycoprotein:

A

adsorbs to tooth, lubrication, bacterial adhesion counter-receptor

131
Q

Fxn of Statherin:

A

stabilize CaPO4 in solution

132
Q

2 bacterial adhesion counter-receptors:

A

Acidic-PRP’s, proline-rich glycoproteins

133
Q

PRP’s and statherin, high or low m.w.?

A

low

134
Q

carrier proteins of Ca2+ in oral cavity:

A

acidic PRP’s

135
Q

Protein to fight C. albicans:

A

Histatic

136
Q

Histatin 1, 3, 5:

A

38, 32, 24

137
Q

TF? sIgA is bacteriacidal.

A

F.

138
Q

Salivary proteins involved in acquired immunity:

A

sIgA, IgG

139
Q

Salivary proteins in innate immunity and host defense:

A

agglutinating factors, antimicrobial proteins, and cationic antimicrobial peptides

140
Q

List agglutinating facotrs:

A

sIgA, mucins, and salivary agglutinins

141
Q

List antimicrobila proteins:

A

cystatins, von Eb gland proteins, P secretory gland proteins (PSP, SPLUNC2), Prolactin induced protein (PIP), secretory leukocyte peptidase inhibitor (SLIP), lysozyme, lactoferrin, lactoperoxidase

142
Q

List cationic antimicrobial peptides:

A

histatins 1,3,5, a/beta defensins, cathelicidin, LL-37

143
Q

mucin w more promiscuous bacteria binding:

A

MUC7

144
Q

Source of lysozyme, lactoferrin, lactoperoxidase:

A

inflammatory cells

145
Q

sIgA:

A

heavy/light/J chains, secretory component (heaviest), first line defense in all mucosal tissues, agglutination of microorganisms, netralize viruses, toxins, enzymes, opsoniztion and mediation of bactericidal activity, interactes with mucin, renders bacteria “mucophilic”,

146
Q

Secretory component of sIgA is composed of:

A

N- and O-linked oligosaccharides (carries all Lewis, siallyl La-epitopes)

147
Q

Fxn of heavy chain of sIgA:

A

binding site ofr certain bacteria (E. coli, Actinomyces naeslundii, Strep. gordonii)

148
Q

Lysozyme is derived from:

A

mainly from granulocytes and monocytes, but also sg’s

149
Q

Fxn of lysozyme:

A

hydrolysis of peptidoglycans in cell wall of gram + bacteria (lysis, cidal)

150
Q

indicator of ongoing inflammation, could be periodontitis or cancer:

A

lactoferrin

151
Q

lactoferrin is derived from:

A

granulocytes

152
Q

Lactorferrin:

A

transferrin family, iron-binding glycoprotien, made by epi cells of sg ducts, in colostrum, milk, tears, bacteriostatic through sequestration of iron, bactericidal through membrane disturbances, host modulation, assoc w pd and caries

153
Q

Is lactoferrin bacteriostatic or cidal?

A

can be either

154
Q

lactoferrin is bactericidal through:

A

membrane disturbances

155
Q

lactoferrin is bacteriostatic through:

A

sequestration of iron

156
Q

Lactoperoxidase is derived from:

A

sg’s (salivary peroxidase) and granulocytes (myeloperoxidase, 30-75%)

157
Q

Lactoperoxidase-thiocynate-H2O2 system is involved in:

A

forms hypothiocynate (OSCN-) oxidation of bacterial enzymes (static or cidal)

158
Q

Where does the thiocynate come from?

A

saliva

159
Q

Where does the H2O2 come from?

A

non-cariogenic bacteria

160
Q

How do cationic antimicrobial peptides kill?

A

inserting into membrane (facilitated by charge), modulates host cell response, directly attack internal targets

161
Q

Disadv to using saliva as a diagnostic tool:

A

lower amt than in blood, conc’s changes, components can be modified

162
Q

miniaturized test devices;

A

micro-arrays, sensors, fluidics, nantoechnology “lab on a chip”

163
Q

What we can measure in saliva:

A

elctrolytes (Ca, K), Ab’s (HIV, Hep A-C), Cytokines, hormones (androgen, cortisol, stradiol, grogesterone, testosterone), Nucleic acids (DNA, RNA, human, mito, microbial, viral), drugs metabolites toxins (alcohol, cotini, phenytoin)

164
Q

Uses of saliva in emergencies:

A

self diagnosis, on site monitoring, epidemics, bioterrorism

165
Q

Pd inflammatory mediators in saliva:

A

IL-1B, IL-6, TNF-a, PGE2

166
Q

Collagen and bone resorption markers in PD:

A

MM8 (collagenase 2), osteoprotegrin (OPG)

167
Q

of proteins in salivary proteome:

A

over 2,000

168
Q

2 forms of SS:

A

primary (sicca syndrome) and secondary (w other AId’s, lupus, RA)

169
Q

Form of SS that is systemic:

A

primary

170
Q

Prevalence of SS:

A

0.2%-0.7% of pop

171
Q

Oral mani of SS:

A

secondary to dry mouth: cervical caries, dry, leathery mucosa

172
Q

Salivary d. mani:

A

swollen sg, parotitis secondary to xerostomia (children)

173
Q

TF? All SS pts lose salivary flow.

A

F

174
Q

Pts w SS may have:

A

blood dyscrasias/ lymphomas, cutaneous vasculitis, lymphadenopathy, primary biliary cirrhosis

175
Q

most serious sequela of SS:

A

lymphoma

176
Q

Dx criteria for SS:

A

2 of 3: dry eyes (ocular staining score), sg inflammation (minor sg biopsy), + serum Ab’s

177
Q

AutoAb’s of SS are produced by:

A

B cells

178
Q

Presence of autoAb’s tells us:

A

patient has disease, levels dont tell us how active the d. is

179
Q

Focus score greater than or equal to __ is indicative of SS:

A

50 lymphocytes / 4 mm2

180
Q

TF? Inflammation is main determining factor in whether a pt will experience dry mouth.

A

F

181
Q

other factors besides inflammation that may cause dryness:

A

apoptosis of epi cells, autoAb’s that inhibit M3R activation

182
Q

Factors contributing to SS:

A

gender, env (viral), genes, innate immune dysfunction, B and T cell abnormalities (adaptive)

183
Q

Why does it affect women more?

A

many immune genes are expressed on X chomosome, mouse wo estrogen shows sg inflammation and increased apoptosis of salivary epi

184
Q

Viruses induce secretion of:

A

Type 1 IFN (elevated in SS salivary tissue), IFN gene dysregulation (inducible gene, labial sg and peripheral blood)

185
Q

Viruses that may play a role in SS:

A

CMV, EBV, HHV6, Human T lymphotropi virus 1, Hep C and D, Enterovirus

186
Q

SS involves both innate and acquired immunity.

A

T

187
Q

These produce high levels of type i IFN following viral activation:

A

dendritic cells in SS salivary tissues express TLR-7 and 9

188
Q

Major producer of inflammatory mediators in SS:

A

macs (inc levels)

189
Q

secrete inflammatory cytokines and express factors that activate adaptive immune cells in SS pts:

A

Salivary gland epi cells (SGEC)

190
Q

Cell type(s) found in Sg biopsy:

A

B and T (% B increases with progression of disease)

191
Q

TF? Both innate and adaptive immunity serve to promote chronic inflammation.

A

T

192
Q

T cells produce:

A

inflammatory mediators, which are elevated in SS salivary tisue

193
Q

Types of T cells in SS tisseu:

A

Th1, Th2, Th17

194
Q

B cell abnormalitites in SS:

A

inc levels of cytokine BAFF (blood and saliva), many different autoAb’s, abnormalities in expression of chemokine receptors that direct B cell migration, high risk of B cell lymphoma

195
Q

Fxn of BAFF:

A

B cells that should die kept alive, secreting their Ab’s, may explain being more prone to lymphoma, may become malignant

196
Q

Biologics (biological products):

A

blood and blood components, gene therapy, tissues, and recombinant therapeutic proteins, may reduce inflammation in SS, diminish cell activation and/or reduce B cell numbers

197
Q

Unstimulated and stimulated salivary flow:

A

0.3-0.4ml/min, 1.5-2.0 ml/min (5 times unstimulated)

198
Q

Easy way to remember relative contributions of the glands:

A

60% subman for unstim and 35% subman or stimulated. 7% for minors always, the rest is parotid

199
Q

Objective criteria for xerostomia/ hypofunction:

A

un: less than or equal to 0.1ml/min, stim: less than or equal to 0.7ml/min

200
Q

Pts will have discomfort/ decay at this salivary flow rate:

A

0.2 ml/min

201
Q

Causes of xerostomia:

A

salivary gland aplasia, water/metabolite loss, iatrogenic (meds, chemo, radiation)

202
Q

Local factors that cause xerostomia:

A

decreased chewing, smoking, mouth breathing

203
Q

Systemic diseases assoc with xerostomia:

A

SS, DM, DI, Sarcoidosis, HIV, HepC, graft vs. host, psychogenic disorders

204
Q

Prevalence of xerostomia:

A

about 30% of pop 65+

205
Q

Mucosal signs of SS:

A

mucositis, desquamation/ sloughing, atrophic mucosa, allergic or contact and lichenoid lesions, candidiasis

206
Q

Signs of SS on tongue:

A

loss of papillae, crenations/ scalloped borders, redness, atrophy, fissures, lobulation

207
Q

Signs of SS on lips:

A

dryness, peeling, fissuring, angular chelitis

208
Q

angular chelitis:

A

fungal infection in corners of mouth, patients who are overclosed, vertical collapse, constant pooling at the side of the mouth

209
Q

Candidiasis:

A

pseudomembranous, red or white, can be scraped away, red underneath, related to hyposalivation, cream cheese consistency, irritated, bleeds at times

210
Q

Classic locations of candidiasis:

A

tongue and soft palate

211
Q

Candidiasis is especially freuqent with patients that use:

A

corticosteroid inhaler

212
Q

Med induced xerostomia;

A

over 500, neural mechanimss, stop drug, regain function, most don’t damage glands,

213
Q

Drugs that lead to xerostomia:

A

anti- cholinergic, hypertensive (ACE inhibitors, angiotensin rec blockers, a/beta adrenergic blockers, diuretics, histamines, opioids, relaxants, antidepressants, antipsychotics

214
Q

Tricyclic anti-depressants block:

A

histaminic, cholinergic, and adrenergic rec sites

215
Q

Antihypertensives that lead to reduced protein in saliva

A

non-selective and beta 1-selective adrenoceptor antagonists

216
Q

Appetite suppressants:

A

inhibit uptake of noradrenaline (NE) and serotonin

217
Q

Pseudophedrine:

A

sympathometic drug, acts directly on alpha-adrenergic receptors

218
Q

central inhibition of salviary output:

A

block signals from forebrain/ hypothalamus going toward the salivary nuclei with a-2-adrenoceptor agonists, serotonin transporters, and NE transporters

219
Q

Peripheral inhibition:

A

anticholinergic muscarinic receptor blockers

220
Q

Radiation is most frequently used for this cancer:

A

scc, malignant epithelial proliferation

221
Q

Tissue that is particularly sensitive to radiation:

A

acinar tissue

222
Q

Flow from these sg’s decreases rapidly in 1st wk after radiation:

A

P and SM, 50-60%, barely measurable at 6-8wks, further decrease for up to 3y

223
Q

Acute phase after radiation:

A

loss of glandular cells and acinar shrinkage

224
Q

Cause of permanent loss of sg function:

A

loss of acinar cells, then fibrosis

225
Q

More sensitive to radiation, serous or mucous?

A

serous (P and SM)

226
Q

TF? Mucous glands typically recover 100% of function.

A

F. 50%

227
Q

Neg effects of sialorrhea:

A

pooling, choking, perioral dermatitis (sores around mouth and chin), infected, tx: drugs or surgery

228
Q

Causes of sialorrhea:

A

GERD, rabies, heavy metal poisoning, anti-psychotics (clozapine), cholinergic agents (AZ, M. gravis,)

229
Q

Tx for sialorrhea

A

botox, surgical removal of part of gland, reposition duct opening

230
Q

Diff dx if salivary flow is greater than or equal to 0.2m/min:

A

Taste disturbances, burning mouth syndrome

231
Q

Diff dx if salivary flow is less than or equal to 0.1m/min:

A

MIX, radiation, SS, other AI d., neurologic and endocrine, infectious d., congenital exocrine gland deficiences

232
Q

Palliative tx for xerostomia:

A

water, biotene, saliva substitutes, oralbalance, different Rx, sugarless candy

233
Q

Required for wax to simulate salivary fxn:

A

neural reflex, requires residual acini

234
Q

Salivary substitutes we can Rx:

A

pilocarpine (salagen), cevimeline HCl (Evoxac)

235
Q

MOA and SE’s of pilocarpine:

A

para agonist, sweating, diarrhea

236
Q

MOA of and SE’s of cevimeline:

A

AcH derivative (activates entire para system), nausea, vomiting, bloating (last only 30m)

237
Q

Most important tx for xerostomia:

A

fluoride: varnish, gel-kam (0.4% Stannous F), prevident (1.1% NaF Rx only), rinses wo alcohol

238
Q

Brought into the lumen through striated ducts:

A

K+

239
Q

AcH pw in acinar cells:

A

AcH, M3R, Gq, PLC, PIP2, DAG and IP3, Ca2+ release from ER

240
Q

NE pw in acinar cells:

A

NE, B-adrenergic, Gs, AC, cAMP

241
Q

Salivary secretion is driven by:

A

electrochemical stimulation

242
Q

Exchangers involved in AcH mediated secretions:

A

Na/H (Nhe1) and Cl/HCO3 (Slc9a1?)

243
Q

Cl- channel into lumen:

A

Tmem16A

244
Q

K+ channel taking K out of BL mem:

A

Ik1 or Sk4 and Maxi-K or Slo (Kcnn4 Kcnma1)

245
Q

Na/K/Cl cotransporter:

A

NKcc1 (slc12a2)

246
Q

basolateral side:

A

Regulation of ion balance

247
Q

apical side:

A

Water channel

248
Q

Tight junctions in acini:

A

leaky, allow passage of water and sodium

249
Q

Drives the flow of Na and water along gradient, creating energy:

A

Cl-, Na bw cells, water bw and through

250
Q

Ca activates:

A

Chloride, K, and Na/K/Cl channels

251
Q

Req for fluid and electrolyte secretion from acinar cells:

A

Ca release

252
Q

Where are ions pumped in bicarbonate mediated secretions?

A

H+ BL, bicarbonate apical

253
Q

bicarbonate mediated secretions, ligand dep or indep?

A

Ligand independent bc we are not talking about a nt

Na/K pump and Na/H exchanger involved.

254
Q

Rec for protein rich secretions:

A

beta adrenergic

255
Q

active ___ leads to protein secretion in the symp pw to protein secretion

A

PKA

256
Q

2 types of protein secretion:

A

exocytosis and vesicular transport

257
Q

Required for packaging high conc of proteins into granules:

A

Ca2+ to shield high density of neg charges (esp. mucins: lare, highly glycosylated, neg charged proteins)

258
Q

Vesical transport:

A

no loss of storage granules, occurs in absence of fluid secretion, can lead to build up of secretory proteinsin duct system, protein composition differs bw granules and vesicles (selective sequestration)

259
Q

Para receptors:

A

M3, M1, alpha-2 adrenergic, Substance P

260
Q

Sym receptors:

A

B2 adreneric or VIP

261
Q

Na is removed principally by:

A

striated duct cells, into glnadular interstitium

262
Q

Degree of hypotonicity is dependent upon:

A

salivary flow rate, stim = higher flow = higher salt conc

263
Q

Removal of NaCl by ductal cells is dependent on:

A

transmembrane gradient for Na by the Na/K ATPase (pump) located in BLl membrane

264
Q

How are Na ions absorbed by ductal cells?

A

from ductal lumen through a Na channel in apical membrane, also remove Cl from saliva in ductal lumen, Cl moves across ductal cell and into interstitium

265
Q

Ion movements in striated duct:

A

Na and H out, K and bicarbonate in

266
Q

What is required for taste recognition?

A

concentrations that reach their taste recognition threshold

Oral Sciences (16 decks)

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