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Epithelial > week 19 epithelial fluid secretion > Flashcards

week 19 epithelial fluid secretion Flashcards

1
Q

which has a greater fluid recover volume? small or large intestine

A

small 7L
Large 1.9L

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2
Q

what disease inhibits fluid reabsorption in the gut?

A

cholera

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3
Q

ion movement across a ‘tight’ epithelial monolayers drives _____ movement

A

water

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4
Q

polarised organisation of channels, pumps, exchangers and junction proteins determines _____ and ______ of water movement

A

direction and movement

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5
Q

how many routes of transepithelial water movement are there

A

2

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6
Q

intracellular movement of water occurs where

A

inside cells

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7
Q

intracellular movement of water occurs within cells and is regulated by what

A

water channels - aquaporins

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8
Q

paracellular movement of water occurs where

A

between cells

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9
Q

paracellular movement of water occurs between cells and is regulated by what

A

tight junction permeability

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10
Q

what are the 2 routes of transepithelial water movement

A

intracellular
paracellular

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11
Q

ENaC draws fluid from where of the cell nd into the blood

A

apical surface of the cell

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12
Q

what pump allows Cl- ions into the cell

A

NKCC

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13
Q

where is the NKCC pump located

A

on the basolateral surface of the cell

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14
Q

cl- accumulates in the ____ of the cell and creates ________ movement of which ion

A

lumen
paracellular movement
Na

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15
Q

Cl- channels = fluid _______

A

secretion

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16
Q

Cl- channels transport from where to where

A

basolateral to apical transport

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17
Q

Na+ channels = fluid _____

A

absorption

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18
Q

Na+ channels transport from where to where

A

apical to basolateral transport

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19
Q

what is the swelling-activated Cl- channel

A

(IClvol)

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20
Q

what does the swelling-activated Cl- channel (IClvol) do
how is it activated

A

activated transiently by osmotic shock
sustained opening does not occur

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21
Q

what is the calcium activated Cl- channel

A

CaCC

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22
Q

what does the Calcium activated Cl- channel do (CaCC)
how is it activated and is it transient?

A

activated by release of intracellular Ca2+ stores. Activity is transient and therefore unlikely to be sustained in development

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23
Q

what is the outwardly rectifying Cl- channel

A

(ORCC)

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24
Q

what does the Outwardly rectifying Cl- channel (ORCC) do
how is it regulated

A

regulated by release of intracellular ATP. Maintains potential by regulated depolarisation to physiological set point

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25
Q

what is the cystic fibrosis transmembrane conductance regulator

A

CFTR

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26
Q

what does the cystic fibrosis transmembrane conductance regulator do
what does it regulate and where

A

best characterised channel due to role in cystic fibrosis disease. Long presumed to be channel regulating fluid secretion in adult lung

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27
Q

what is the voltage dependant Cl- channel

A

CLCN

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28
Q

what does the voltage dependant Cl- channels (CLCN) do
where is it and what process development does it follow (organ)

A

recently characterised in lung. Expression pattern follows the process of lung development

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29
Q

what is the CFTR a member of

A

member of the ATP binding cassette (ABS) glycoprotein superfamily

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30
Q

what is the kDa of CFTR

A

170kDa

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31
Q

how many _ transmembrane domains is CFTR composed of

A

2x 6 transmembrane domains

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32
Q

how many nucleotide binding domains does CFTR have

A

2

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33
Q

what are the 2 nucleotide binding domains that CFTR has (common to all ABC proteins)

A

NBD1 and NBD2

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34
Q

how many R domains are there in CFTR

A

1

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35
Q

what is a unique feature of CFTR

A

has one single domain of highly charged amino acids

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36
Q

in CFTR, the R domain is a regulatory site containing several ______ sites for what protein kinases

A

phosphorylation sites
protein kinases A and C

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37
Q

activation of CGTR Cl- conductance requires ___ binding to what domains

A

ATP binding
to the NBD domains and phosphorylation of the R domain

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38
Q

how many stages are there in the normal cycle of regulation of CFTR

A

6

39
Q

STAGE 1 of normal cycle of regulation of CFTR
what state is the channel in

A

channel is inactive

40
Q

STAGE 2 of normal cycle of regulation of CFTR
what does cAMP activate

A

cAMP activation of protein kinase A phosphorylates R domain

41
Q

STAGE 3 of normal cycle of regulation of CFTR
What does ATP bind to

A

ATP binds to NBD1 and NBD2

42
Q

STAGE 4 of normal cycle of regulation of CFTR
what is hydrolysed

A

ATP is hydrolysed

43
Q

STAGE 5 of normal cycle of regulation of CFTR
what happens to the channel
what ion is conducted

A

channel opens and conducts Cl-

44
Q

STAGE 6 of normal cycle of regulation of CFTR
what happens to the R domain and subsequently the channel

A

dephosphorylation of the R domain inactivates the channel

45
Q

what mutation in the NBD1 region of CFTR causes cystic fibrosis

A

Phenylalanine 508 (deltaF508 or F508del)

46
Q

in delta508 CFTR (mutation that causes cystic fibrosis) what occurs

A

no fluid in the airway secretion
- dry lung
- sticky mucus
- pathogen colonisation

47
Q

In CLCN1-7 what is the channel opening gated by

A

membrane potential

48
Q

IN CLCN1-7 where is it found

A

epithelia
muscle
nerve tissue
plants

49
Q

CLCN2 expressed in epithelium is activated at ______ cell membrane potentials

A

negative (hyperpolarised)

50
Q

in CLCN 1-7 is composed of how many transmembrane domains

A

10

51
Q

in CLCN1-7 the 10 transmembrane domains dimerise to form how many pores

A

2

52
Q

in CLCN 1-7 the 10 transmembrane domains dimerise to form 2 pores, each pore is ________

A

voltage gated

53
Q

CLCN1 mutation causes what

A

myotonia

54
Q

in the CLCN1 mutation causing Myotonia - what does this cause

A

failure of muscles to relax after contraction as cells remain depolarised

55
Q

what does a mutation in the CLCN5 mutation cause

A

Dent’s disease

56
Q

in the CLCN5 mutation causing dent’s disease - what does this cause

A

fluid transport problems in kidney resulting in kidney stones, calcium and protein loss in urine

57
Q

CLCN2 and CLCN3 are developmentally expressed in what foetal organ

A

lung

58
Q

CLCN2 and CLCN3 are developmentally expressed in the feotal lung and control what

A

control lung fluid volume during development

59
Q

where is the ENaC channel always found within epithelia

A

secretory epithelia
lung, kidney gut, salivary duct, sweat duct

60
Q

how many subunits is the ENaC composed of

A

3

61
Q

what are the 3 subunits ENac composed of

A

alpha
beta
gamma

62
Q

in ENaC a genetic alpha knockout results in what

A

lethal at birth due to flooding of the lungs

63
Q

in ENaC knockout of beta or gamma subunits results in what

A

not lethal but is associated with a marked reduction in the rate of Na+ transport

64
Q

in ENaC what is the dominant pore forming subunit

A

alphaENaC

65
Q

ENaC is composed of alpha, beta, and gamma but how many subunits are there

A

4
2 alpha subunits

66
Q

In ENaC what is the extracellular loop rich in

A

cystine

67
Q

In ENaC within the extracellular loop what type of tertiary structure is it rich in

A

CSSC sulphur cross linking

68
Q

what residue is involved in channel opening and closing within ENaC

A

histidine glycine residue

69
Q

in ENaC what residue rich region serves as a binding motif for NEDD4

A

proline tyrosine

70
Q

proline tyrosine residue rich region which srves as a binding motif for what

A

NEDD4

71
Q

proline tyrosine residue rich region which srves as a binding motif for NEDD4 is what kind of ligase

A

ubiquitin ligase

72
Q

proline tyrosine residue rich region which serves as a binding motif for NEDD4, a ubiquitin ligase which targets the subunit for membrane removal and what kind of degradation

A

proteolytic

73
Q

what is ENaC inhibited by

A

amiloride

74
Q

What is ENaC activated by

A

Beta2 adrenergic agonist

75
Q

ENaC conductance is induced by what

A

catecholamines

76
Q

pseudohypoalosteronism (PHA) and Liddle’s syndrome are diseases associated with loss and gain of function mutations on what channel subunits

A

ENaC

77
Q

PHA disease is associated with resistance to what hormone

A

aldosterone

78
Q

As PHA is a disease associated with resistance to aldosterone what ion imbalance does this lead to

A

increased Na excretion
- dehydration
- hypotension
-hyperkalaemia
- metabolic acidosis

79
Q

PHA disease is most evident in what organ

A

kidney

80
Q

most lethal form of PHA is caused by loss of funtion mutations in what subunit in ENaC

A

alpha
beta
gamma

81
Q

Liddle’s syndrome is charcterised by what

A

hypertension
hypokalaemia
metabolic alkalosis
repressed aldosterone secretion

82
Q

results from gain of function mutations on what terminus domain if beta and gamma subunit in ENac

A

C terminal domain

83
Q

In liddle’s syndrone
results from gain of function mutations in the C terminal domain of beta or gamma ENaC which result in the deletion of how many amino acids in the proline tyrosine rich PY domain

A

45-75 amino acids

84
Q

results from gain of function mutations in the C terminal domain of beta or gamma ENaC which result in the deletion of how many amino acids in the deletion of 45-75 amino acids from what domain

A

proline-tyrosine rich PY domain

85
Q

what ubiquitin ligase promotes internalisation and degradation of PY motif

A

NEDD4

86
Q

channel activating proteases (CAP) increase what activity

A

ENaC

87
Q

what increases ENaC activity

A

Channel Activating Proteases (CAP)

88
Q

secreted CAP inhibitors block what and in what

A

secreted CAP inhibitors block CAP activity in concentrated ASL

89
Q

how many extracellular CAPD are found in ASL

A

3

90
Q

three extracellular CAPS dound in ASL can cleave what

A

ENaC

91
Q

three extracellular CAPS found in ASL can cleave ENaC does what to its activity

A

increases the activity of ENaC

92
Q

High ASL dilutes secreted what and secreted what

A

dilutes secreted protease inhibtors
dilutes secreted CFTR agonists

93
Q

Low ASL concentrates secreted CAP protease inhibitors and secreted _____ agonists

A

CFTR

Epithelial (12 decks)

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