Membranes, Nerve, Muscle and Neurophysiology COPY Flashcards

1
Q

What is the nernst equation with regards to its importance in membrane physiology?

A

The nersnst equation describes the electrical potential that opposes the diffusion of a molecule across a membrane. Ions will want to move in the directoin that brings them closer to this potential (equilibrium).

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2
Q

For each of the following molecules, indicate which is more prevalent inside vs. outside the cell:

  1. Sodium
  2. Potassium
  3. Chloride
  4. Magnesium
  5. Bicarbonate
  6. Phosphate
  7. Amino acids and proteins
  8. Glucose
  9. Lipids (e.g. cholesterol, phospholipids)
A
  1. Outside
  2. Inside
  3. Outside
  4. Inside
  5. Outside
  6. Inside
  7. Inside
  8. Outside
  9. Inside
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3
Q

How does urea move through the cell membrane?

A

Urea is highly permeable through cell membranes.

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4
Q

What are the selecitivty filters of the following channels?

  1. Na
  2. K
A
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5
Q

How will the rates of diffusion differ for facilitated vs. simple diffusion?

How does this differ when considering physiologic membranes?

A

Facilitated will reach a maximum, likely due to the rate at which the proteins in the channels can change shape.

Simple diffusion will always increase rate of diffusion in a linear fasion.

Membrane permeability will affect the movement of the substance in question when in a physiologic medium.

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6
Q

Name the three factors that affect rate of diffusion of charged molecules?

A
  1. Concentration
  2. Nernst potential
  3. Pressure
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7
Q

What is the membrane potential of most membranes?

A

-70mV

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8
Q

What channels are present in the cell that contribute to the resting membrane potential?

A

Na/K-ATPase

K leak channels - these allow free movement of potassium. Since the Na/K pump moves positive ions out of the cell in greater quantity to those coming in, the potassium will reach and equilibrium potential under resting conditions.

This is why changing ECF potassium concentrations can change the resting membrane potential. The resting potential becomes more negative with low ECF potassium as there is a lower concentration gradient for potassium to move into the cell.

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9
Q

Explain the events that occur in the membrane of cells during action potential with reference to sodium and potassium channels.

A
  1. ‘Fast’ sodium channels open which are inactive at -70mV but are activated and open following stimulus.
  2. These become inactive again (through a different mechanism) when the membrane potential becomes positive again.
  3. They return to their resting state only when the membrane has reached resting potential again.
  4. Potassium channels will also be activated when there is an action potential but they are much slower to open and therefore the net movement of sodium is much quicker than potassium during depolarisation.
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10
Q

How does ECF calcium concentration affect membrane exitability?

A

It is thought that Ca binds to the exterior of sodium channels and affects the voltage required to open them. This is how the calcium affects threshold potentials.

e.g. Hence why low calcium causes hyperexitability as it means depolarisation is more likely to occur.

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11
Q

What is the value of the normal threshold potential?

A

15-30mV

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12
Q

Why are cardiac action potentials so much longer than nerve action potentials?

A

L-type calcium channels are present in the physiology of cardiac muscle contraction. These act in a similar way to sodium channels but are much slowe to open and close.

Potassium channels in cardiac muscle also seem to open and close slower.

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13
Q

How might action potentials be elicited by a stimulus?

A

Either with a large stimulus or a more frequent stimuli.

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14
Q

What is the molecular mechanims of the refractory period?

A

This is the period in which the sodium (or calcium) channels inactivation gate is closed. This will only re-open once the membrane reaches its resting potential again.

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15
Q

Explain the following terms in relation to skeletal muscle anatomy:

I bands

A bands

Z disk

Sarcomere

Titin

A

I = the layers of actin only

A = where actin and myosin overlap

Z = protein filament that attaches to actin

sarcomere = the space between z-discs

Titin = the springy filament that connexts the z-disk to myosin

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16
Q

Where in the actomyosin complex is ATPase activity located?

A

In the myosin head.

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17
Q

What are the structural elements of the actin filament?

A

F-actin = the main structural element tha contains ADP molecules at binding sites

tropomyosin - this covers the binding sites

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18
Q

What are the components of the troponin complex?

A

I - binds to actin

t = binds to tropomyosin

c = afinity for calcium

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19
Q

How many calcium ions can be bound by each troponin C molecule?

A

4

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20
Q

Explain the cross-bridge theory of muscle contraction

A
  1. Calcium binds to troponin C exposing the F-actin binding sites
  2. ATP –> ADP + P by the ATPase on the myosin molecule which results in the head tilting towards the binding site.
  3. Upon binding the power stroke occurs.
  4. ADP + P leave the myosin
  5. A new ATP binds to the myosin which allows it to detach from the actin filament.
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21
Q

What is the relationship of actin overlap to tension that can be created through a muscle?

A

If there is too much overlap then less tension is produced.

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22
Q

Explain the following terms:

  1. Multiple fibre summation
  2. Frequency summation
A

Summation is the addition of contractions to increase intensity of contraction

  1. Increased umber of motor units that fire at the same time
  2. Increasing the frequency at which motor units fire
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23
Q

What is the mechanism by which calcium entry into a cell results in the movement and exocytosis of vesicles?

A

Calcium activates Ca2+-calmodulin–dependent protein kinase, which, in turn, phosphorylates synapsin proteins that anchor the acetylcholine vesicles to the cytoskeleton of the presynaptic terminal. This process frees the acetylcholine vesicles from the cytoskeleton and allows them to move to the active zone of the presynaptic neural membrane adjacent to the dense bars

24
Q

How many Ach molecules are required to activate sodium channels on the motor end plate?

A

2

25
Q

Explain the process by which Ach binding to receptors on the motor end plate results in muscle contraction

A

Ach opens ligand-gated sodium channels that create a local end plate potential which then opens voltage gated sodium channels leading to an action potential.

26
Q

What clears Ach from the synapse? What is the chemical process by which this is achieved?

A

Ach esterase - splits Ach into acetate and choline via hydrolysis. The choline can be re-absorbed and further Ach formed.

27
Q

How do the following drug classes/disease states impact on the NMJ?

  1. NMB agents (e.g. atracurium)
  2. Nystigmine, nicotine, pyristigmine?
  3. MG
A
  1. They block the Ach receptors on the initial sodium channels
  2. These prevent the breakdown of Ach by Ach esterase
  3. Usually thought to be due to antibody production agains the motor end plates (in the congential condition it may be that the receptors are just not present or are deficient in some way).
28
Q

What is the resting membrane potential of a skeletal muscle?

A

-80 - -90Mv

29
Q

What receptors/channels are responsible for caclium release from the sarcoplasmic reticulum?

A

Dihydropyridine (DHP) [voltage-gated] receptors result in release of caclium through ryanodine receptors that are present in the sarcoplasmic reticulum.

30
Q

What molecule binds calcium in the sarcoplasmic retuculum?

A

Calseqeusterin

31
Q

How does malignant hyperthermia occur?

A

Halogenated anaesthetics can result in activation of the DHP or RyR.

32
Q

What is the mechanism of action of dantrolene?

A

It antagonises the RyR preventing calcium release from the sarcoplasmic reticulum.

33
Q

What is the key difference in how smooth muscle contraction differs from skeletal muscle contraction?

A

Smooth muscle does not contain troponin. Instead calcium entry into the cell minds to calmodulin. This activates myosin light chain kinase (MLCK) which then phosphorylates the myosin head (converts ATP to ADP + P).

34
Q

What enzyme is required for smooth muscle relaxation?

A

Myosin phosphatase

35
Q

Which ion is responsible for generation of smooth muscle action potentials (c.f. skeletal muscle)?

A

Calcium

36
Q

Where in the spinal chord does the symphathetic chain originate?

A

T1 - L2

37
Q

What type of symphathetic fibre ultimately results in SNS stimulation of end organ?

A

C-fibres.

38
Q

Which nerves in the body have parasympathetic activity?

A

III (occulomotor), VII (facial), IX (glossopharyngeal), X (vagus), pelvic

39
Q

How is acetylcholine synthesised?

A
40
Q

Describe the steps in norepinephrine (and epinephrine) synthesis

A
41
Q

How is norepinephrine cleared from synapses?

A
  1. Re-uptake
  2. Diffusion to other site
  3. Enzymatic breakdown
    - Monoamine oxidases in the synamse
    - COMT in tissues
42
Q

What types of membrane proteins do muscarinic and nicotinic receptors tend to be coupled to?

A

Muscarinic = GPCRs

Nicotinic = ion channels (e.g. NMJ)

43
Q

What is the difference in receptor type that is activated by nEP vs. EP?

A

nEP has a greater ability to activate alpha

EP has a more balanced effect

44
Q

Which adrenoreceptor results in vasoconstriction?

A

alpha 1

45
Q

Which adrenoreceptor results in intestinal relaxation?

A

A1 and B2

46
Q

Which adrenoreceptor is inhibitory within the adrenergic system?

A

Alpha 2

47
Q

Which adrenoreceptor results in vasodilation?

A

beta 2

48
Q

Which adrenoreceptor results in bronchodilation?

A

beta 2

49
Q

Which adrenoreceptors are generally found within the cardiac system (excluding blood vessels)?

A

beta 1

50
Q

What are the main factors involved in contol of cerebral blood flow?

A
  1. CO2 and subsequent H+ concentration
  2. O2 concentration
  3. astrocytes
51
Q

Over what range does the brains autoregulatory mechanism work well?

A

60-150mmHg

52
Q

What structure forms the blood-brain barrier?

A

Astrocyte foot processes (aka. astroglial cells)

53
Q

Which space does the CSF live in?

A

The subarachnoid space

54
Q

Where is CSF formed?

A

Choroid plexus

55
Q

What is the normal CSF pressure?

A

10mmHg

56
Q

Why are the arachnoidal villi important for preventing increased cerebral pressure and in what circumstance could this be overriden?

A

They are the ‘valves’ that allow CSF out and into the venous sinuses. They may become blocked by WBCs, bacteria etc. in inflammatory disorders.

Congential hydrocephalus - one mechanism could eb a lack of arachnoidal villi.

57
Q

What are the three components of the Cushing’s reflex and why does this occur?

A
  1. Irregular breathing (brainstem compression)
  2. Peripheral vasoconstriction (brain increases MAP to increase cerebral perfusion pressure)
  3. Bradycardia (reflex bradycardia)