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CVS 2023 > Cellular and molecular events COPY > Flashcards

Cellular and molecular events COPY Flashcards

1
Q

What sets up resting membrane potential?

A

K+ permeability

Cardiac myocytes permeable at rest

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2
Q

Flow of K+

A

Na+K+ATPase sets up concentrations
K+ is high in cell so moves out of cell
Makes inside negative relative to outside

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3
Q

Equilibrium potential for K+

A

When chemical and electrical gradients result in no net movement of K+

(Chemical gradient draws K+ out of cell, Negative electrical charge pulls K+ back into cell)

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4
Q

Why is resting membrane potential not Ek?

A

Small permeability to other ions at rest

BUT K+ is main determinant of RMP

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5
Q

Ek vs RMP

A 
Ek = -95mV
RMP = -80 to -90mV
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6
Q

Special features cardiac myocytes

A

Fire action potentials

Electrically coupled to allow syncronized contraction

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7
Q

What does action potential trigger?

A

Increase in Ca2+ in cytoplasm

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8
Q

What triggers action potential?

A

Depolarisation

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9
Q

Whys is Ca2+ required?

A

Allows actin and myosin interaction (binds to Troponin C)

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10
Q

Length of action potentials

A

SA node and Cardiac ventricle have much longer action potentials than axons/skeletal muscle

100ms vs 0.5ms

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11
Q

Ventricular cardiac action potential steps

A

Depolarisation = opening of Voltage gated Na+ channels (curve goes positive)
Transient outflow of K+ (curve dips slightly negative)
Opening of Ca2+ channels = plateau (some K+ channels open)
Ca2+ channels inactivate, V gated K+ channels open (curve goes back to resting membrane)

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12
Q

What causes depolarisation?

A

Opening of V gated Na+ channels

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13
Q

What causes slight dip in membrane potetial? (initla repolarisation)

A

Transient outflow of K+

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14
Q

What sustains plateau phase?

A

Open V gated Ca2+ channels

some K+ channels are open

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15
Q

What causes repolarisation?

A

Ca2+ channels inactivate

V gated K+ channels open - K+ moves out

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16
Q

3 phases of Ventricular action potential

A

Na+ influx
Ca2+ influx (K+ efflux)
K+ efflux

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17
Q

SA node action potential difference

A

No stable Resting membrane potential
Slow depolarisation after each cycle
Na+ doesn’t cause fast depolarisation - Ca2+ does

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18
Q

3 phases of SA node action potential

A 
Pacemaker potential (If - funny current) from influx of Na+ (slow depolarisation)
Opening of V gated Ca2+ channels (fast depolarisation)
Opening of V gated K+ channels (repolarisation)
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19
Q

Pacemaker potential job

A

Initial slope to threshold - funny current (If)

Activated at negative membrane potentials (lower than -50mV) - more negative more activation

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20
Q

How does SA node achieve transient inflow of Na+?

A

HCN channels
Hyperpolarisation-activated Cyclic Nucleotide-gated channels
allow influx of Na+

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21
Q

Types of Ca2+ channels SA node

A

L-type and Transient (T ) type

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22
Q

How is upstroke achieved SA node?

A

Opening of V gated Ca2+ channels

23
Q

How is down stroke (repolarisation) achieved in SA node?

A

Opening V gated K+ channels (leaves)

24
Q

Innervation SA node

A

No innervation needed

Natural automaticity

25
Q

Membrane potential SA node

A

UNSTABLE (pacemaker potential, funny current)

26
Q

Action potentials through heart speed

A

SA node = fastest

27
Q

Action potential journey

A 
SA node 
Across atria
AV node
Bundle of His
Purkinje fibres 
Ventricle contraction
28
Q

Pacemaker of heart?

A

SA node

sets rhythm

29
Q

AP’s through heart

A

SA node and AV node - fast

Atrial muscle, ventricular muscle and purkinje fibres - slower

30
Q

What is responsible for contraction?

A

Spread of action potential

31
Q

Problems with action potential firing

A

too slow - bradycardia
fail - asystole
too quickly - tachycardia
random - fibrillation

32
Q

Hyperkalaemia

A

High plasma conc (>5.5mmol/L)

33
Q

Hypokalaemia

A

Low plasma conc (<3.5mmol/L)

34
Q

why are cardiac myocytes sensitive to change in K+?

A

k+ permeability dominates membrane potential

35
Q

Hyperkalaemia effects

A

Ek = less negative
Membrane potential depolarises
Inactivates some of Na+ channels
Slows upstroke

36
Q

Risks hyperkalaemia

A

Heart stops - asystole

Initial increase in excitability (depolarised)

37
Q

Extent hyperkalaemia

A

Mild: 5.5 - 5.9 mmol/L
Moderate: 6.0 - 6.4 mmol/L
Severe: > 6.5mmol/L

38
Q

Treatment hyperkalaemia

A

Calcium gluconate
Insulin and glucose

(causes cells to uptake K+)
**Heart needs to be pumping

39
Q

Effects of hypokalaemia

A

Lengthens action potential

Delays repolarisation

40
Q

Problems hypokalaemia

A

Longer action potentials can cause Early After Depolarisation (EAD’s)
Oscillations in membrane potential
Ventricular fibrillation

(remember shaking in hypothermia like osscilations)

41
Q

Excitation contraction coupling initial step

A

Depolarisation opens L type Ca2+ channels in T tubules

42
Q

What does Ca2+ entering cytosol cause in cardiac cells?

A

Opens Calcium induced calcium release (CICR) channels in SR

43
Q

What happens after CICR channels open?

A

Ca2+ binds to troponin C
Conformational change shifts tropomyosin
Binding site revealed on actin = myosin can bind

44
Q

How do cardiac myocytes relax?

A

Ca2+ pumped into SR (via SERCA)

Some exits via membrane (Ca2+ATPase, Na+Ca2+ exchanger)

45
Q

How is tone of blood vessels controlled?

A

Contraction and relaxation of vascular smooth muscle cells

tunica media, arteries arterioles and veins

46
Q

Excitation contraction coupling smooth muscle cells initial stimulation

A

Noradrenaline activates a1 receptors

or depolarisation opening V gated Ca2+ channels

47
Q

What does a1 receptor do?

A

Activates Gaq to produce second messanger IP3

48
Q

What does IP3 do?

A

Binds to receptors on sarcoplasmic reticulum

Initiates release of Ca2+

49
Q

What does Ca2+ once released from cell? (smooth muscle)

A

Binds to calmodulin

50
Q

what does calmodulin do?

A

Activates Myosin light chain kinase (MLCK)

51
Q

What does MLCK do?

A

Phosphorylates myosin light chain = allows interaction with actin

52
Q

How does contraction stop in smooth muscle?

A

Myosin light chain phosphatase dephosphorylates the myosin light chain

PKA phosphorylates myosin light chain kinase = inactive

53
Q

How is contraction inhibited? (smooth muscle cell)

A

PKA (protein kinase A) phosphorylates MLCK and inhibits it

54
Q

Cardiac muscle vs smooth muscle excitation and contraction

A

Cardiac:
Action potential allow Ca2+ entry
More Ca2+ then comes from SR
Ca2+ binds to TROPONIN C

Smooth muslce:
Depolarisation/activation of a-adrenoreceptors
Increased intracellular Ca2+
Ca2+ binds to Calmodulin
Activates MLCK - phosphorylates myosin light chain

CVS 2023 (26 decks)

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