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ESA2 > CVS - Electricals > Flashcards

CVS - Electricals Flashcards

1
Q

What is the funny current?

A

Slow inward current of Na+ that is activated at membrane potentials more negative than -50mV

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2
Q

What is different about some characteristics of the SAN AP compared to a ventricular myocyte?

A
  • Spontaneous
  • Funny current
  • Unstable membrane potential
  • No fast Na channels (slow upstroke)
  • Upstroke is Ca2+ channels not Na+
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3
Q

What is the pacemaker potential?

A

Stage 4 - slow depolarisation to threshold of VOCCs

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4
Q

At what mV do T and L type Ca2+ channels open in the SAN AP?

A

T -50mV

L - -40mV

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5
Q

What are the funny current channels called?

A

HCN - Na+ channels

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6
Q

Why is the SAN pacemaker of the heart?

A

As it is the fastest cell type in the hear to depolarise so sets the rhythm.

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7
Q

Why is the heart particularly susceptible to a change in K+ plasma conc?

A
  • Cardiac membrane potential is particularly sensitive to K (close to EK+) so a change in the EC K+ conc will change the membrane potential
  • Many types of K+ channels in heart and some behave in peculiar ways
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8
Q

What effect does high plasma K+ conc have on the heart?

A

Asystole

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9
Q

What is the effect of hyperkalaemia on the ventricular AP?

A

Will shorten AP
Will depolarise myocyte - so slowing the upstroke of the AP and inactivating some of the Na+ channels - less Na channels available to contribute to the AP

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10
Q

What might you see with hyperkalaemia before asystole? How do you you treat hyperkalaemia? Why wouldn’t this treatment work in asystole?

A

May see a temporary increase in excitability

Treat with calcium gluconate - reduces excitability of myocytes so decreases the risk of arrhythmias

Wouldn’t work in asystole as needs to be pumped around the body

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11
Q

What are the effects of hypokalaemia on the ventricular AP?

A

Lengthens AP
Causes EADs (probably due to reactivation of Ca2+ channels)
Oscillations in MP
VF

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12
Q

What happens when an AP arrives at a cardiac myocyte?

A

1) Arrives via GAP junction
2) At T tubules - activates VOCCs (L type Ca channels/DHP receptors (same thing))
3) Ca2+ influx (25%)
4) Activated RyRs (close link with DHPRs)
5) CICR - Ca2+ binds with troponin C on tropomyosin and conformation change moves tropomyosin away from the myosin binding site on actin - myosin head binds etc.

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13
Q

What is normal plasma K+ concentration kept between?

A

3.5 - 5.5mM/L-1

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14
Q

What are the 4 stages of the sliding filament theory?

A

1) High energy configuration - Myosin attached to ADP + Pi and head is cocked - attaches to the actin filament
2) Working stroke - ADP and Pi released as myosin head pivots and bends and moves the actin filament towards the M line 5nm
3) Low energy configuration - ATP binds to myosin and the cross bridge detaches
4) Release of Pi causes the cocking of myosin head

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15
Q

What mechanisms return the IC Ca2+ levels back to normal post AP?

A
  • SERCA (most)
  • Na Ca ATPase
  • NCX

Also calmodulin has an enhancing effect on Ca Na ATPase

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16
Q

How does excitation contraction coupling occur in SMCs?

A

1) Depol opens VOCCs
2) Ca2+ in binds to CaM - activates it
3) CaM binds to MLCK and activates it
4) MLCK phosphorylates the light chain of myosin head (increases its ATPase activity
5) This enables myosin binding to actin and can slide across
6) Myosin dephosphorylated by MLCPhosphatase

17
Q

What is the relevance of the regulatory light chain on the myosin head in SMC contraction?

A

It must be phosphorylated to allow actin-myosin binding for contraction to occur

18
Q

How can SMC contracted be inhibited?

A

By phosphorylation of MLCK by PKA - inhibits phosphorylation of the MLC and therefore inhibits contraction - inhibits GalphaS GPCR via beta 2 adrenergic receptor on SMC e.g. some blood vessels

(contraction is via alpha adrenergic receptors e.g. on vessel walls)

19
Q

Which enzyme is constitutively active MLCK or MLCP? How can it be inhibited and what happens?

A

MLCP is - inhibited by PKC (G-alpha q GPCR alpha adrenoceptor) - so releases the activity of MLCP and allows MLC to be phosphorylated –> contraction

20
Q

What is the effect of vagus nerve acting at M2 receptors on the heart?

A 
Decreased HR (negative chronotropic effect)
Decreased AVN conduction velocity (negative dromotropic effect)

Vagus nerve has most effect on SAN and AVN but also decreases ionotropy (force of contraction) and luisitropy (relaxation)

21
Q

What is the effect of the parasympa and sympa nervous system on pacemaker potentials?

A

Sympa - increases the slope of pacemaker potential - increases rate of depol
Para - decreased the slope of the pacemaker potential - decreases rate of depol

22
Q

How does sympa increase slope of pacemaker potential and how does para decrease it?

A

Sympa - via G alpha S GPCR cAMP

Para - via G alpha I GPCR decreased cAMP and increases K+ conductance

23
Q

How does sympa NS increase ionotropy in the heart? (force of contraction) (3)?

A

1) Phosphorylation of Ca2+ channels increases Ca2+ entry during plateau phase of AP - more RyRs activated
2) Increased uptake of Ca2+ in SR so more released to bind to troponin C
3) Increased sensitivity of contractile machinery to Ca2+

24
Q

Do vessels receive parasympathetic input?

A

Not really - only erectile tissue

25
Q

Coronary, liver and skeletal muscle vasculature have which two adrenergic receptors?

A

Beta 2 and alpha 1

26
Q

What is vasomotor ton and how does this allow for vasodilation to occur?

A

As vessels only under sympa control - normally have a degree of muscle tone - decrease the sympa input - decreases the muscle tone = vasodilation. Increase the sympa input - increase the tone = vasoconstriction

27
Q

What is the role of Beta-2 receptors on coronaries, liver, and skeletal muscle vasculature? What effect does this have - vasodilation or constriction?

A

They have a high affinity to circulating adrenaline so adrenaline will bind preferentially to beta-2 receptors At higher concentrations adrenaline will also bind to alpha-1 receptors.

Activating beta-2 adrenoceptors on vascular smooth muscle causes vasodilation.

28
Q

How do beta-2 adrenergic receptors cause vasodilation on binding of circulating adrenaline?

A

Via G alpha s GPCR - activating AC, cAMP, opens K+ channels - inhibits MLCK, causes hyperpolarisation - less contraction - relaxation of smooth muscle

29
Q

What is the main thing that increases blood flow to skeletal muscle and coronary muscle - metabolites or beta-2 activation by adrenaline?

A

Metabolites have a more important effect on vasodilation than activation of beta-2 receptors

30
Q

Give some examples of local metabolites that lead to vasodilation in coronary and skeletal muscle?

A

CO2
H+
K+
Adenosine

31
Q

How is blood pressure controlled moment to moment? What can happen in pathology?

A

Baroreceptors in the aortic arch and carotid sinus detect blood pressure changes and alter via afferent nerves to the brain - to the brain centre in the medulla that alters via para or sympathetic NS efferents. In pathology the BP set point can change e.g. in hypertension

32
Q

What happens if low blood pressure is detected by atrial receptors?

A

Atrial receptors detect low blood pressure and signals the kidneys to increase H20 retention to increase BP

33
Q

How does salbutamol work?

A

B2 agonist - increases smooth muscle relaxation in the airways in asthma

34
Q

How does dobutamine work? When would you use it?

A

B1 agonist - increases ionotropy, and sometimes chronotropy - used in cardiogenic shock

35
Q

What is a sympathomimetic drug?

A

Drug that mimics the endogenous agonists of the sympathetic nervous system

36
Q

How does propranolol work? What is the problem with it? Why is atenolol potentially better?

A

beta-1 and beta-2 antagonist - slows HR, decreases ionotropy, but increases bronchoconstriction - side effect

Atenolol has more selectivity for beta-1 receptors so less risk of bronchoconstriction

37
Q

How does prazosin work?

A

alpha- 1 antagonist - vasodilation - antihypertensive

38
Q

How does pilocarpine work?

A

M agonist - contraction of pupil used in treatment of glaucoma

39
Q

How does atropine work?

A

alpha - muscarinic antagonist In eye - dilates pupil, in heart increases HR, bronchial dilation

ESA2 (37 decks)

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