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BS2014 - Phys Pharm II > Dr. Micheson > Flashcards

Dr. Micheson Flashcards

1
Q

For the quantity ‘Charge’ what is the:

1) Quantity symbol
2) Unit
3) Unit symbol
4) Equivilent

A

1) Q
2) Coulomb
3) C
4) A s

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2
Q

For the quantity ‘Current’ what is the:

1) Quantity symbol
2) Unit
3) Unit symbol
4) Equivilent

A

1) I
2) Ampere
3) Amp
4) C/s

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3
Q

For the quantity ‘Potential difference’ what is the:

1) Quantity symbol
2) Unit
3) Unit symbol
4) Equivilent

A

1) V, E
2) Volt
3) V
4) J/C

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4
Q

For the quantity ‘Energy (work)’ what is the:

1) Quantity symbol
2) Unit
3) Unit symbol
4) Equivilent

A

1) -
2) Joule
3) J
4) CV

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5
Q

For the quantity ‘Power’ what is the:

1) Quantity symbol
2) Unit
3) Unit symbol
4) Equivilent

A

1) -
2) Watt
3) W
4) J/s, AV

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6
Q

For the quantity ‘Resistance’ what is the:

1) Quantity symbol
2) Unit
3) Unit symbol
4) Equivilent

A

1) R
2) Ohm
3) Ω
4) V/A

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7
Q

For the quantity ‘Conductance’ what is the:

1) Quantity symbol
2) Unit
3) Unit symbol
4) Equivilent

A

1) G
2) Siemens
3) S
4) 1/Ω, A/V

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8
Q

For the quantity ‘Capacitance’ what is the:

1) Quantity symbol
2) Unit
3) Unit symbol
4) Equivilent

A

1) C
2) Farad
3) F
4) C/V

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9
Q

What is ohms law?

A

V=I.R

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10
Q

What does Q=?

A

Q=C.V

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11
Q

What does N=?

A

N=C.V/F

N = number of moles of charge moved

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12
Q

What does dV/dt=?

A

dV/dt=1/C

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13
Q

What is the specific capacitance of biological membranes?

A

1 μF per cm^2

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14
Q

What is the elementary charge (e) on 1 electron?

A

1.6x(10^-19)C

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15
Q

What is Avagadro’s constant?

A

6.023x10^23

Number of atoms in 1 mol

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16
Q

What is Faraday’s constant (F)?

A

9.65x10^4 charge on 1 mol of electrons

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17
Q

What is an action potential?

A
  • Active process requiring energy to maintain electrochemical gradients (eg. K+, Na+ ATPase)
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18
Q

What is passive (electrostatic) conduction?

A
  • No energy is required

- Usually post-synaptic potentials

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19
Q

When does current flow?

A
  • If there is a potential difference (V) (i.e. difference in charged particles (Na+/K+ ions))
  • If they are connected by a conductor
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20
Q

What is current?

A
  • Flow of charged particles (ions)

- Rate of flow of charge —> I=G.V

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21
Q

What effects the amount of current through a conductor for a given potential difference?

A
  • I is proportionally related to the conductor’s conductance
  • I is inversely proportional to its resistance (Ohms law)
  • I=V/R
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22
Q

Which ions have larger concentrations in the extracellular space?

A
  • Ca2+
  • Na+
  • Cl-
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23
Q

Which ion has larger concentrations in the intracellular space?

A
  • K+
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24
Q

How does a lipid bilayer act as a) Resistor b) Capacitor

A

a) Resistance depends on the number of open ion channels (conductors) - resistance is lower when more are open
b) The lipid bilayer is an excellent capacitor as it can store charge difference between the two sides of the membrane

25
Q

Define capacitance

A

1) The store of charge that builds up on the membrane for a given voltage.
2) It can also be thought of as the quantity of charge required to change
membrane potential by a given value.
3) Membrane capacitance acts to slow changes of membrane potential

26
Q

What is a capacitor?

A

2 conductors separated by a thin insulator

- Best when the insulator is very thin - more stored charge

27
Q

How does a capacitor work?

A
  • +ve one side -ve the other, attracts across the narrow insulator meaning it can store charge because of the electrostatic attractions
28
Q

What links capacitance to cell size and myelination

A
  • C ∝ SA/insulator thickness
  • SO capacitance is directly proportional to size, and inversely proportional to insulator thickness
  • Size - larger SA means larger charge can be stored so bigger capacitance (larger cells - larger capacitance)
  • Myelination - this increases the insulator thickness, thicker the insulator lower the capacitance and the charge that can be stored
29
Q

What gives the charge stored on a capacitor (Q)?

A

Q=C.V (capacitance x voltage)

30
Q

How is current (I) linked to capacitance?

A

I=C.δV/δt (rate of change of voltage with respect to time)

31
Q

How are membrane capacitance and resistance linked

A

Membrane capacitance (Cm) and resistance (Rm) are in parallel with each other

32
Q

What kind of cells does Vm rise slowest in?

A

Large cells and cells with high membrane

resistances

33
Q

What equations give the time constant?

A

τ = R m . Cm
(Vm =Vmax . (1-e(-t/RC) τ = R ))
time (t) for Vm to change by 63% of to change by 63% of Vmax

34
Q

Typically, in neurons, what are the time constants?

A

20-50ms

35
Q

When does change in Vm increase linearly

A

For subthreshold stimuli

36
Q

What effect does a larger current have?

A

Changes potential more rapidly

37
Q

What’s the main principle of cable theory?

A

In long cellular processes (eg axons, dendrites and muscle fibres), passive responses decrease with distance from stimulus.

38
Q

Define length constant gamma

A

distance from current
injection point (x) when voltage signal has
decreased to ~ 37 %
( V = V e^(-x/λ))

39
Q

In a good conductor what happens to the length constant

A

It’s longer

40
Q

What are the three components of resistance in a neuron?

A

Rm, (membrane) Ra (axon) & Rext (extracellular fluid)

41
Q

Describe leaky cable theory

A
  • Rm is constant, but Ra and Rext increase with distance – resistances in series are additive. As current flows along cytoplasm some of it leaks across the membrane.
  • Flow of current along a nerve process depends on leakiness of membrane (dependent on Rm) relative to resistance of cytoplasm (Ra).
  • Larger cell diameter means lower Ra
42
Q

What is epilepsy?

A

A chronic disease that leads to repetitive seizures due to temporary abnormal CNS neuronal activity. It may involve loss of consciousness and tonic or clonic convulsions

43
Q

What are the symptoms and classification

A

Over 50 syndromes have been described. They can be divided according to the source of the seizure into:

1) focal or partial syndromes – abnormal electrical activity localised to specific region of CNS.
2) generalised syndromes – activity in both hemispheres

Epilepsies can also be divided based upon causative (aetiological) considerations.

1) Idiopathic syndromes – mostly genetic in origin
2) Symptomatic or acquired syndromes for which there is an associated neurological disturbance e.g. damage from stroke, head trauma, tumour…

44
Q

How is it diagnosed

A

Diagnosis is based on medical history and electroencephalography (EEG) recordings

45
Q

What are EEG recordings

A
  • Picking up extraneuronal
  • measuring on electrical brain activty
  • made by array of electrodes on scalp
  • CNS signals and cortex
  • Field potentials - groups of neurones
  • From pairs of electrodes
  • Alpha relaxed wakeful, beta active wakeful, delta and theta are low frequency drowsy or early sleep
  • 1 to 30 Hz
  • Epilepsy high frquency sharp spikes
  • Limited, MRI and PET scans can see deeper
46
Q

Describe idiopathic epilepsy syndrome

A
  • Inherited
  • Hundreds of mutations in sodium channel protein have been identified in patients with Generalised epilepsy with febrile seizures plus (GEFS+) an initially mild, dominantly inherited epilepsy
  • Characterized by febrile seizures in childhood that progresses to generalized epilepsy in adults - Can cause brain damage, neuronal cell death
47
Q

Describe the role of sodium channel mutations on epilepsy

A

A wide variety of functional effects on channel properties have been reported – location and functional effect are both critical

Gain of function mutations in excitatory neurons – mutations increase sodium current.

Loss of function mutations in inhibitory interneurons – mutations decrease sodium current

Net effect in both cases, is an increase of excitatory neuronal output that can spread to cause a seizure

48
Q

Give an ecample of muta can increase cahnnel actiity

A

A common finding of gain of function sodium channel mutations is a slowing of inactivation and a persistent current. - larger sodium entry - greater firing of AP

Q54 mice provide a genetic model of seizures due to Na channel dysfunction

Mice develop frozen posture seizures after 3 months

Older mice develop spontaneous tonic-clonic seizures – with limb jerking and excess salivation.

Q54 mice die prematurely – only 25% survive beyond 6 months

Seizure onset correlates with high frequency spiking initially in hippocampus, which then spreads to cortex.

Q54 mice have a normally developed hippocampus, but once seizures start there is extensive neural loss .

In this case - Na channel mutations likely cause persistent neuronal depolarisation, hyperexcitability and cell death.

49
Q

How does mutatioj cause a loss of channel activity

A

Loss of function activity but LOCATION is in the GABAergic inhibitory neurons meaning overal INCREASE in excitability - hyperexcitability - leads to epilepsy in patienst with GEFS+ & other epilepsy
No different in Pyramidal neurons
Half number of Na 1.1 - sodium channel

50
Q

What is caused by mutations in K+ ions

A

BNFC characteris by recurrent brief generalised seizures, start early in life day 4 and stop about 3 months but greater risk for later epilep in life

  • inherited mutations on ACh sensitive K+ channels (M-current channels)
  • Inhibiting K+ currents
  • Decreasing K+ its making cell more prone to firing action potentials
51
Q

What two genes are required to form functional M-current?

A

KCNQ2 & KCNQ3

52
Q

How much is M current reduced by

A

20-30% leading to neuronal hyperexcitability causing BNFC

53
Q

What is MS

A

CNS disease due to axon demyelination
MS is an autoimmune disease that leads to damage to myelin or oligodendrocytes of myelinated CNS neurons
Clinical presentation is quite varied
Classical symptoms are blurred vision, muscle weakness, muscle spasms and loss of sensation
Risk factors are both genetic (women and caucasian) and environmental.
A lot not understood

54
Q

Diagnosed

A

MRI scans - break down of blood brain barrier, heavy metals build up

55
Q

How does demyelination cause MS

A

Demyelination increases membrane capacitance and decreases membrane resistance – alters local current circuits.

  • Rm causes length constant to shorten
  • Cm makes membrane time constant longer and more current is required for membrane depolarisation
  • Demylination slows AP conduction velocity.
  • Ion channels may redistribute along axon in completely demyelinated regions – essentially axon has conduction properties of an unmyelinated axon.
56
Q

When does total conduction block occur

A

Total conduction block occurs if current from healthy node is not sufficient to depolarise neighbouring nodes to threshold potential – this is the main cause of symptoms for MS patients.

APs have longer duration – increases refractory periods and so APs blocked at higher frequencies.

Demyelination makes axons more prone to fire spontaneous APs. Neurons excitability can be increased or mechanical stimuli can cause ectopically generated APs.

57
Q

Describe cross talk

A

Reduced insulation between axons means that current from an AP in one axon causes depolarisation of the axon of neighbouring cell.

The resulting AP is propagated in both directions.

58
Q

SUMMARY OF NEUROLOGICAL DISEASES

A

Epilepsy is a collection of disorders resulting from hyperexcitability of some neuronal networks.
Idiopathic (genetic) syndromes are commonly associated with mutations in ion channels.
Epilepsy associated mutations in Na channels can increase or decrease Na currents – depending upon location.
Mutations in KCNQ2 and KCNQ3 K channel subunits decrease M-current amplitudes.

Na and K channel mutations all result in neuronal hyperexcitability (and cell death).

MS is due to demyelination and defects in AP conduction of CNS neurons.
Demyelination alters the passive conduction properties of axons – decreases Rm and increases Cm.

MS and epilepsy demonstrate importance of both passive conduction and ion channel function in AP conduction.

59
Q

SUMMARY

A

Action potentials are constantly regenerating electrical signal and are propagated by passive conduction of current.
• Factors that influence longitudinal flow of current (Ra, Rext) or rate of depolarisation (Rm and Cm) have a large impact on conduction velocity.
• Myelination enhances conduction velocity by insulation of the axon (increases Rm at internodes and thus length constants), and by shortening time constants for depolarisation at nodes of Ranvier (decreasing Cm and Rm).

BS2014 - Phys Pharm II (5 decks)

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