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cvpr exam i copy > 11, 12. EC Coupling and Ca++ Handling > Flashcards

11, 12. EC Coupling and Ca++ Handling Flashcards

1
Q

What is this series of events?:
• Ca2+ enters via DHPR (“L-type Ca2+ channel”) and activates RyR2 to cause large flux of Ca2+ from SR into myoplasm.
• Ca2+ activates contraction by binding to troponin on thin filaments.
• Ca2+ is removed from the myoplasm by:
(i) SERCA2 pump located in longitudinal SR (2 Ca2+ per cycle); Ca2+ diffuses within SR to terminal cisternae, where it binds to calsequestrin (low affinity, high capacity)
(ii) NCX Na+/Ca2+ exchanger in junctional domains of plasma membrane and t-tubules.

A

excitation, contraction, and relaxation of Cardiac muscle

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2
Q

The sequence of events during excitation, contraction and relaxation of cardiac muscle cells is:

  1. • Ca2+ enters via _____ and activates RyR2 to cause large flux of Ca2+ from SR into myoplasm.
  2. • Ca2+ activates contraction by binding to ____ on thin filaments.
  3. • Ca2+ is removed from the myoplasm by:
    (i) _____ located in longitudinal SR (2 Ca2+ per cycle); Ca2+ diffuses within SR to terminal cisternae, where it binds to calsequestrin (low affinity, high capacity)
    (ii) NCX Na+/Ca2+ exchanger in junctional domains of plasma membrane and _____
A
  1. DHPR (“L-type Ca2+ channel”)
  2. troponin
    i. SERCA2 pump
    ii. t-tubules
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3
Q

The sequence of events during excitation, contraction and relaxation of cardiac muscle cells is:

  1. • Ca2+ enters via DHPR (“L-type Ca2+ channel”) and activates _____ to cause large flux of Ca2+ from SR into myoplasm.
  2. • Ca2+ activates contraction by binding to troponin on ______.
  3. • Ca2+ is removed from the myoplasm by:
    (i) SERCA2 pump located in _____ (2 Ca2+ per cycle); Ca2+ diffuses within SR to terminal cisternae, where it binds to calsequestrin (low affinity, high capacity)
    (ii) _____ in junctional domains of plasma membrane and t-tubules.
A
  1. RyR2
  2. thin filaments
    i. longitudinal SR
    ii. NCX Na+/Ca2+ exchanger
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4
Q

The sequence of events during excitation, contraction and relaxation of cardiac muscle cells is:

  1. • Ca2+ enters via DHPR (“L-type Ca2+ channel”) and activates RyR2 to cause large flux of Ca2+ from ____ into _____.
  2. • ___ activates contraction by binding to troponin on thin filaments.
  3. • Ca2+ is removed from the myoplasm by:
    (i) SERCA2 pump located in longitudinal SR (2 Ca2+ per cycle); Ca2+ diffuses within SR to terminal cisternae, where it binds to _____ (low affinity, high capacity)
    (ii) NCX Na+/Ca2+ exchanger in _____ of plasma membrane and t-tubules.
A
  1. SR into myoplasm
  2. Ca2+
    i. calsequestrin
    ii. junctional domains
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5
Q

What is a junctional domain?

A

junction btw the terminal cisternae of the SR and the plasma membrane

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6
Q

What is the junction btw the terminal cisternae of the SR and the plasma membrane called?

A

a junctional domain

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7
Q

What is a t-tubule?

A

plasma membrane invaginations

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8
Q

What plays the more important role: SERCA or NCX?

A

SERCA bc the SR surrounds each myofibril and this will req less energy

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9
Q

What is heart failure?

A

insufficient cardiac output, typically due to lack of contractile force

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10
Q

What is insufficient cardiac output, typically due to lack of contractile force called?

A

heart failure

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11
Q

How do cardiac glycosides work? Give an example of one.

A

inhibit Na/K ATPase and thus reduce extrusion of Ca++ via NCX; digitalis

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12
Q

Where is norepinephrine released from?

A

sympathetic nerve terminals

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13
Q

Epi and norepi act to:

  1. Increase Heart Rate (positive chronotropy) by _____
  2. Increase Contractile Force (positive inotropy)
  3. Increase Rate of Relaxation (positive lusitropy)
A

raising the firing rate of pacemaker cells in the SA node

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14
Q

Epi and norepi act to:
1. Increase Heart Rate (positive chronotropy) by raising
the firing rate of pacemaker cells in the SA node.
2. _____
3. Increase Rate of Relaxation (positive lusitropy)

A

Increase Contractile Force (positive inotropy)

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15
Q

Epi and norepi act to:
1. Increase Heart Rate (positive chronotropy) by raising
the firing rate of pacemaker cells in the SA node.
2. Increase Contractile Force (positive inotropy)
3. _____

A

Increase Rate of Relaxation (positive lusitropy)

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16
Q

Four important targets for PKA in cardiomyocytes are?

A
  • The L-type Ca2+ channel
  • RyR2
  • Phospholamban (PLB)
  • Troponin
17
Q

_____ of the L-type Ca2+ channel increases the amplitude of the L-type Ca2+ current, increasing:

(i) the trigger for activation of _____
(ii) the ____ content

A

Phosphorylation

i. RyR2
ii. SR Ca2+

18
Q

Phosphorylation of the _____ increases the amplitude of the L-type Ca2+ current, increasing:

(i) the trigger for activation of RyR2 and
(ii) the SR Ca2+ content

A

L-type Ca2+ channel

19
Q

Phosphorylation of the L-type Ca2+ channel increases the _____, increasing:

(i) the trigger for activation of RyR2 and
(ii) the SR Ca2+ content

A

amplitude of the L-type Ca2+ current

20
Q

Phosphorylation of ____ increases its activation by Ca2+.

A

RyR2

21
Q

Phosphorylation of RyR2 increases its activation by ____.

A

Ca2+

22
Q

____ inhibits SERCA2 Ca2+ pumping activity.

A

PLB

23
Q

PLB inhibits _____ Ca2+ pumping activity.

A

SERCA2

24
Q

PLB inhibits SERCA2 _____ pumping activity.

A

Ca++

25
Q

What is Timothy Syndrome?

A
  • genetic disorder causing arrhythmias, syncope, and sudden death
  • causes immune deficiencies, cognitive abnormalities, autism
  • de novo mutations of CaV1.2
  • TS and TS2 variants have AV block, suppress voltage-dependent inactivation; prolonged Q-T intervals and PVT
26
Q
  • genetic disorder causing arrhythmias, syncope, and sudden death
  • causes immune deficiencies, cognitive abnormalities, autism
  • de novo mutations of CaV1.2
  • TS and TS2 variants have AV block, suppress voltage-dependent inactivation; prolonged Q-T intervals and PVT
A

Timothy Syndrome

27
Q

What is Brugada Syndrome?

A
  • mutations of cardiac sodium channels NaV1.5, KChip2, and ankyrin
  • significantly shortened Q-T interval
  • large reduction in the magnitude of L-type Ca2+ current
28
Q

What is another name for Brugada Syndrome?

A

Sudden Unexplained Death Syndrome

29
Q
  • mutations of cardiac sodium channels NaV1.5, KChip2, and ankyrin
  • significantly shortened Q-T interval
  • large reduction in the magnitude of L-type Ca2+ current
A

Brugada Syndrome

30
Q

What is Catecholaminergic Polymorphic Ventricular Tachycardia (CPVT)?

A
  • dominant mutations of RyR2 or recessive calsequestrin2 mutations
  • no ECG abnormalities
  • abnormalities upon exercise or infusion of catecholamines
  • Activation of beta-adrenergic receptors causes arrhythmias
31
Q
  • dominant mutations of RyR2 or recessive calsequestrin2 mutations
  • no ECG abnormalities
  • abnormalities upon exercise or infusion of catecholamines
  • Activation of beta-adrenergic receptors causes arrhythmias
A

Catecholaminergic Polymorphic Ventricular Tachycardia (CPVT)

32
Q

How is CPVT treated?

A

beta-blockers

33
Q

_____ blocks RyR2, but at doses too high to be clinically useful.

A

Tetracaine

34
Q

Tetracaine blocks ____, but at doses too high to be clinically useful.

A

RyR2

35
Q

_____ is a class 1C anti-arrhythmic that blocks cardiac sodium channels.

A

Flecainide

36
Q

Flecainide is a class ____ anti-arrhythmic that blocks cardiac sodium channels.

A

1C

37
Q

Flecainide is a class 1C anti-arrhythmic that blocks cardiac ____ channels.

A

sodium

38
Q

What is calcium-dependent inactivation (CDI)?

A

inactivation of the L-type Ca++ channel on its cytoplasmic side, determined by Ca++ concentration

helps maintain a constant SR Ca++ content

39
Q

What helps to maintain a constant SR Ca2+ content?

A

calcium-dependent inactivation (CDI)

cvpr exam i copy (29 decks)

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