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Y2S1 - Homeostasis > Homeostasis 1 > Flashcards

Homeostasis 1 Flashcards

1
Q

What proportion of cell membrane is lipids?

A

42%

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2
Q

What proportion of cell membrane is proteins?

A

55%

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3
Q

What proportion of cell membrane is carbohydrates?

A

3%

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4
Q

What primary function does the cell membrane function?

A

Divides IC and EC fluid

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5
Q

What kinds of substances freely diffuse across the membrane?

A

Lipid soluble substances

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6
Q

What kind of substances require transport proteins?

A

Small molecules and ions

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7
Q

What kind of substances require endocytosis?

A

Large molecules

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8
Q

What are the three fundamental methods of crossing the cell membrane?

A

Diffusion, transport proteins and endocytosis

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9
Q

What are the three fundamental types of transporters?

A

Carriers, pumps and channels

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10
Q

Why are carriers described as secondary active?

A

Reliant on primary active proteins that are reliant on ATP, i.e. they are 2 steps away from ATP

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11
Q

What do pumps rely on?

A

ATP

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12
Q

What is the most common kind of channel transporter?

A

Voltage gated

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13
Q

Comment on the turnover and speed of channel transporters.

A

Very high turnover - million to 10 million ions per second

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14
Q

What is the patch clamp technique used for?

A

Measuring currents across a very small region of the cell membrane

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15
Q

Describe the patch clamp technique.

A

Pipette with 1µm tip attached to cell and filled with salt solution and silver wire. Wire attaches to reference electrode in EC space. Suction applied to create high resistance seal with the cell membrane, and currents are measured across that patch

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16
Q

What else can the patch clamp technique be used for?

A

Measurement of the whole cell PD - enough suction can rupture the cell

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17
Q

What are the drawbacks to the patch clamp technique?

A

Identification of channels is difficult, regulatory properties are unknown, physiological function is difficult to discern

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18
Q

What equation defines protein channel regulation?

A

SEE PAD 5

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19
Q

How do you measure Vm?

A

Insert electrode through PM containing salt solution that cannot leave; difference in voltage between solution and reference electrode outside of cell calculated as Vm

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20
Q

What is the distribution of Na across the cell?

A

15mM IC; 150mM EC

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21
Q

What is the distribution of K across the cell?

A

150mM IC; 5 mM EC

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22
Q

What is the distribution of anions across the cell?

A

65mM IC; 0mM EC

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23
Q

What maintains the K/Na distribution?

A

Na/K ATPase

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24
Q

What does the restriction of anions IC allow?

A

Potential gradient to drive PM proteins

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25
Q

What two methods does Na/K ATPase contribute to Vm?

A

Direct - 20% - electrogenic transport protein that creates a loss of +ve charge; indirect - through IC K and Na changes

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26
Q

Define the Nernst equation.

A

SEE PAD 25

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27
Q

What is E-K?

A

minus 90.1 mV

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28
Q

What is E-Na?

A

plus 61 mV

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29
Q

What is Vm?

A

minus 70 mV

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30
Q

Define the Goldmann equation.

A

SEE PAD 26

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31
Q

What kind of disease is long QT syndrome and myotonia?

A

Channelopathies

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32
Q

What are the five stages that channelopathies can be interfered with?

A

Conduction, regulation, trafficking, processing, production

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33
Q

What do long QT syndromes lead to?

A

Arrhythmias and sudden death

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34
Q

What is the incidence of long QT syndrome?

A

1 in 10,000 to 1 in 15,000

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35
Q

How many forms of long QT syndrome are there?

A

7, possibly 8

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36
Q

What mutations cause long QT-1?

A

LOF KCNQ1

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37
Q

What are KCNQ?

A

K channels

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38
Q

What does LOF stand for?

A

Loss of function

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39
Q

What does GOF stand for?

A

Gain of function

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40
Q

Why doesn’t LOF KCNQ1 stop all K transport?

A

More than one K channel, so K still moves, just takes longer to repolarise

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41
Q

What regulates KCNQ1?

A

KCNE1

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42
Q

What mutations cause long QT-5?

A

LOF KCNE1

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43
Q

What mutations cause LQT-2?

A

LOF HERG K channel

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44
Q

What mutations cause LQT-3?

A

GOF SCN5A Na channel

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45
Q

What mutations cause LQT-4?

A

LOF ankyrin B

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46
Q

What mutations cause LQT-6?

A

LOF KCNE2

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47
Q

What mutations cause LQT-7?

A

LOF Kir2.1

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48
Q

What is myotonia?

A

Muscle stiffness through hyper-excitability of skeletal muscle by delayed relaxation

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49
Q

What is the incidence of myotonia?

A

1 in 23,000 to 1 in 50,000

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50
Q

What causes myotonia congenita?

A

LOF CLCN1

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51
Q

What two types of myotonia congenita are there?

A

Thomsen’s AD and Becker’s AR

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52
Q

What does AD stand for?

A

Autosomal dominant

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53
Q

What does AR stand for?

A

Autosomal recessive

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54
Q

What is another name for paramyotonia?

A

K aggravated myotonia

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55
Q

What is another name for K aggravated myotonia?

A

Paramyotonia

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56
Q

What mutation causes paramyotonia?

A

GOF SCN4A

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57
Q

What is SCN4A?

A

Na-v 1.4

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58
Q

What is the MOA of paramyotonia?

A

Inactivation of gated Na channel, thus more Na enters muscle and depolarisation is prolonged

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59
Q

What is the treatment for paramyotonic CLC1 mutations?

A

Mexilitene

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60
Q

What is mexilitene used to treat?

A

Paramyotonia

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61
Q

What is the MOA of mexilitene?

A

Na channel blocker

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62
Q

What is the genetic inheritence of CF?

A

AR

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63
Q

What does CF stand for?

A

Cystic fibrosis

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64
Q

What is CF?

A

Disease of electrolyte transport in epithelial

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65
Q

What is the incidence of CF sufferers?

A

1 in 2500

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66
Q

What is the incidence of CF carriers?

A

1 in 20

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67
Q

What is the MOA of CF?

A

Problems with trafficking channels to the cell surface

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68
Q

What six organs are affected by CF?

A

Airways, liver, pancreas, small intestine, reproductive tract and skin

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69
Q

How are the airways affects by CF?

A

Clogging and infection

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70
Q

How is the liver affected by CF?

A

Blockage of small bile ducts and problems with liver function in 5%

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71
Q

How is the pancreas affected by CF?

A

Blockage of ducts prevents secreation of digestive enzymes in 65%

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72
Q

How is the small intestine affected by CF?

A

Obstruction due to thick content in 10% of newborns

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73
Q

How it the reproductive tract affected by CF?

A

Absence of vas deferens in 95% of males, thus infertile

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74
Q

How is the skin affected by CF?

A

Excess secretion of NaCl via sweat glands

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75
Q

What does NBD stand for?

A

Nucleotide binding site

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76
Q

What is the R site on a channel?

A

Regulatory part

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77
Q

How many CFTR mutations have been identified?

A

1600

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78
Q

How many CFTR mutations can cause CF?

A

1000

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79
Q

Where are 70% of patients’ CFTR mutations?

A

Delta F508

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80
Q

What is the lung pathology of CF?

A

Viscous muscous airway, recurrent bacterial infections, antibiotic resistance, inflammation, tissue degeneration, common cause of death

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81
Q

Outline normal NaCl secretion in upper airway.

A

SEE PAD 27

82
Q

How does the normal mucuous protective layer form?

A

Water flows past mucosal cell layer with Cl flow

83
Q

When was Liddle’s syndrome first described?

A

1963

84
Q

What is the inheritence of Liddle’s syndrome?

A

AD

85
Q

What characterises Liddle’s syndrome?

A

Na retention, fluid retention, hypertension, hypokalaemia, metabolic alkalosis, low renin and aldosterone levels

86
Q

What is the MOA of Liddle’s syndrome?

A

Increased Na reabsorption, increased H2O reabsorption, increased K secretion, increased H secretion

87
Q

What causes Liddle’s syndrome?

A

Mutation in the COOH tail of ENaC leading to insertion, but not endocytic removal from the apical cell surface

88
Q

What is the incidence of malignant hyperthermia?

A

1 in 10,000 to 1 in 50,000

89
Q

What is the genetic inheritence of malignant hyperthermia?

A

AD

90
Q

What is malignant hyperthermia?

A

Abnormal response to anaesthesia

91
Q

What is the mortality rate of malignant hyperthermia if not treated?

A

80%

92
Q

What is the mortality rate of malignant hyperthermia if treated?

A

10%

93
Q

What is tachypnea?

A

Rapid breathing

94
Q

What are the symptoms of malignant hyperthermia?

A

Tachypnea, low plasma O2, high plasma CO2, tachycardia, hyperthermia, rigidity, sweating, shifts in BP

95
Q

What happens to sufferers of malignant hyperthermia if not treated?

A

Respiratory and lactic acidosis, muscular rigidity, muscle breakdown, severe hyperkalaemia, cardiac and neuronal hyperexcitability

96
Q

What is the physiological reason for malignant hyperthermia?

A

Uncontrolled muscle contraction, excessive ATP hydrolysis, hypermetabolic state muscles

97
Q

What is RyR1?

A

Skeletal muscle ryanodine receptor

98
Q

What does MH stand for?

A

Malignant hyperthermia

99
Q

What mutations cause MH?

A

RyR1 GOF - increases P-0 of Ca channels

100
Q

What is the P-0 of a ion channel?

A

Opening probability

101
Q

What anaesthetic triggers a malignant hyperthermic attack?

A

Halothene

102
Q

What does GOF mutation to RyR1 do?

A

Increases sensitivity to halothene

103
Q

What is the treatment of MH?

A

Dantrolene - inhibits RyR1, IV hydration, diuretic - stops kidney damage, NaHCO3 - counter acidosis, hyperventilation

104
Q

What is episodic ataxia type II?

A

Irregular uncontrolled muscle contraction

105
Q

What is the genetic inheritence of episodic ataxia type I and II?

A

AD

106
Q

What mutation causes episodic ataxia type I?

A

KCNA1 (K-v)

107
Q

What mutation causes episodic ataxia type II?

A

CACNA1A (Ca-v)

108
Q

When is the average onset of episodic ataxia type I?

A

20-30 years

109
Q

When is the average onset of episodic ataxia type II?

A

Child to teens

110
Q

What symptoms characterise episodic ataxia type I?

A

Ataxia, dizziness

111
Q

What symptoms characterise episodic ataxia type II?

A

Ataxia, vertigo, nausea, headache

112
Q

How long are episodic ataxia type I attacks?

A

Brief

113
Q

How long are episodic ataxia type II attacks?

A

30mins - 24hours

114
Q

Where is CACNA1A?

A

Purkinje cells, granule cells, cell bodies, cerebellum, exocytotic NT release

115
Q

What is used to treat episodic ataxia?

A

Acetazolomide

116
Q

What type of drug is acetazolomide?

A

Carbonic anhydrase inhibitor

117
Q

What is acetazolomide used to treat?

A

Episodic ataxia

118
Q

What causes the predominant symptoms of influenza?

A

Respiratory pathogens disturb fluid balance in the respiratory tract

119
Q

How do viruses distrupt the fluid balance in the respiratory tract?

A

Knock out Na channels

120
Q

What proteins are on the basolateral surface of the lining of the respiratory tract?

A

NKCC2, K/Na ATPase, ROMK

121
Q

What is tetrodotoxin?

A

Kind of neurotoxin - guanidium neurotoxin

122
Q

What is guanidium neurotoxin also known as?

A

Tetrodotoxin

123
Q

Characterise the potency of tetrodotoxin.

A

10,000 times stronger than cyanide - nM levels required for death

124
Q

Where is tetrodotoxin found?

A

Produced by marine bacteria - held in invertebrates, amphibians and fish

125
Q

How can tetrodotoxin be accidentally ingested?

A

Incorrect Fugu preparation - pufferfish

126
Q

What marine creatures commonly have tetrodotoxin in their bodies?

A

Pufferfish, blue-ringed octopus

127
Q

What are the symptoms of tetrodotoxin ingestion?

A

Numbness of lips and tongue, facial parasthesia, headache, nausea, dizziness, diarrhoea, vomiting, increased paralysis, respiratory paralysis, death in 20mins to 8 hours

128
Q

What does TTX stand for?

A

Tetrodotoxin

129
Q

What is the treatment for tetrodotoxin ingestion?

A

Mechanical ventilation - no anti-venom because TTX binds too strongly

130
Q

What does TTX act upon?

A

Na channel

131
Q

What does the TTX inihibtion of Na channels cause?

A

Failure of neurotransmission, reduction in release of NT, loss of sensation and muscle paralysis, respiratory paralysis

132
Q

Outline the variable sensitivy of the body to TTX.

A

Brain + muscle - sensitive, heart - insensitive; change Na-v 374 from cysteine to tyrosine in the heart leads to sensitivity

133
Q

What three breast cancer metastatic genes have been identified?

A

Cell cycle markers, adhesion markers, motility factors

134
Q

What is the difference in Ca concentration IC and EC?

A

10,000 fold - 100nM indside, 10mM outside

135
Q

What keeps the Ca concentration IC and EC stable?

A

Ca/Na exchanger, Ca ATPase

136
Q

Why is it important that IC Ca concentrations are kept so low?

A

Important secondary messenger, so too much would result in a lack of sensitivity

137
Q

What does the Ca/Na exchanger do ionically?

A

Swaps Na outside for Ca inside - 3Na:1Ca

138
Q

What does the stoichiometry of the Ca/Na exchanged mean?

A

When at equilibrium and combined with membrane potential, the 10,000 fold Ca gradient is maintained

139
Q

What is NCX?

A

Na/Ca exchanger

140
Q

What three kinds of Ca pump are there?

A

PMCA, SERCA, SPCA

141
Q

What is PMCA?

A

Ca ATPase

142
Q

What is SERCA?

A

Ca ATPase

143
Q

What is SPCA?

A

Ca ATPase

144
Q

What does PMCA stand for?

A

Plasma membrane Ca pump (ATPase)

145
Q

What does SERCA stand for?

A

Smooth endoplasmic reticulum Ca pump (ATPase)

146
Q

What does SPCA stand for?

A

Secretory pathway Ca pump (ATPase)

147
Q

What does PMCA do?

A

Pump Ca out of the cell

148
Q

What does SERCA do?

A

Pump Ca out of the cytoplasm and into SER

149
Q

What does SPCA do?

A

Pump Ca out of the cytoplasm and into Golgi apparatus

150
Q

What four channels are involved in Ca signalling?

A

VOCC, ROCC, SOCC and mechanically activated Ca channels

151
Q

What does VOCC stand for?

A

Voltage operated Ca channel

152
Q

What does ROCC stand for?

A

Receptor operated Ca channel

153
Q

What does SOCC stand for?

A

Store operated Ca channel

154
Q

Where are VOCC found, and how are they activated?

A

Excitable cells, activated by depolarisation

155
Q

Where are ROCC found, and how are they activated?

A

Secretory cells and nerve terminals, activated by binding of agonist

156
Q

How are SOCC activated?

A

Activated following the depletion of stores

157
Q

Where are mechanically operated Ca channels found, and how are they activated?

A

Any cells that respond to deformation - activated by that deformation

158
Q

What does failure to migrate and aggregate cells lead to?

A

Cell, tissue and organism dysfunction/death

159
Q

What are cadherins?

A

Calcium dependent cell surface molecules

160
Q

How many cadherins do L cells express?

A

2

161
Q

How were cell adhesion molecules discovered?

A

Monoclonal anti-bodies

162
Q

Describe the structure of cadherins.

A

Monomeric integral membrane glyco proteins, 720-750 a/a

163
Q

What happens to cadherin when Ca binds?

A

Change from floppy to rigid

164
Q

What link cadherins to cytoskeleton?

A

Catenins

165
Q

What do catenins do?

A

Bind cadherins to the cytoskeleton

166
Q

Where is e-cadherin expressed?

A

Early embryo

167
Q

Where is n-cadherin expressed?

A

Replaces e-cadherin in the neural tube

168
Q

What do selectins do?

A

Bind specific carbohydrate groups

169
Q

Are selectins Ca dependent?

A

Yes

170
Q

What are selectins involved in?

A

Neutrophil trapping

171
Q

What is diapedesis?

A

Ability of white blood cells to squeeze through the capillary wall

172
Q

How are selectins involved in neutrophil trapping?

A

P-selectin slow white cells down, others drag it down

173
Q

Describe Ca INDEPENDENT CAMs.

A

Numerous, N-CAMS are the major form (neural)

174
Q

What are Ca independent CAMs involved in?

A

Homophilic, ECM and cell binding

175
Q

How are Ca independent CAMs generated?

A

From a single gene, aternative forms deriven by splicing and post-translational glycosylation

176
Q

Describe the structure and classes of integrins.

A

Dimers - 16 alpha and 8 beta types

177
Q

What do integrins do?

A

Bind the cytoskeleton, causing outside-in or inside-out activation of signalling pathways

178
Q

Are integrins Ca dependent?

A

No

179
Q

What does FAK stand for?

A

Focal adhesion kinase

180
Q

What is FAK regulated by?

A

Ca binding

181
Q

What does FAK do?

A

Recruits/activates multiple tyrosine kinases to inhibit focal adhesions

182
Q

When is FAK activated?

A

On formation of focal adhesions

183
Q

In what important pathway does FAK function?

A

Anoikis - attachment dependent cell death

184
Q

What is mammalian cell motility mainly based upon?

A

Actin

185
Q

What is the cellular cortex?

A

Layer just inside the PM that convey structural support

186
Q

What happens during cell migration?

A

Cortex aids PM tension, signals cause local actin reorganisation, cortex transmits tension, cell polarity emerges, leading edge toward signal, myosin II aids tail retraction

187
Q

What two features comprise the leading edge?

A

Ruffling and retrograde actin transport

188
Q

Describe leading edge ruffling.

A

Forms in front and ‘crashes’ backwards, acts like arms grabbing monkey bars

189
Q

What is responsible for nucleation of actin filaments?

A

ARP complexes

190
Q

Which end of actin filaments is associated with a cluster of proteins?

A

Minus end

191
Q

What does the minus end of actin filaments serve as?

A

Seam for further growth

192
Q

What angle do actin filament branches cross link?

A

70 degrees

193
Q

Along with ARP compexes, what else congregates at the leading edge?

A

Cofalin and capping proteins

194
Q

What form low density focal adhesions?

A

rac1, cdc42

195
Q

What form high density focal adhesions?

A

RhoA, actin-myosing interaction

196
Q

Characterise low density focal adhesions.

A

Immobile

197
Q

Characterise high density focal adhesions.

A

Sliding in the membrane

198
Q

Name three motility signals.

A

Netrins - soluble; CAMs/ECM - insoluble; Fibronectin/crest cells

199
Q

Define the equation for water flux into/out of a cell.

A

SEE PAD 37

200
Q

Why is cell volume important?

A

Structural integrity + cellular protein functioning

Y2S1 - Homeostasis (2 decks)

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