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FHB exam one > Heart 6 > Flashcards

Heart 6 Flashcards

1
Q

Function of the sarcolemma

A

Propagation of action potentials; controls calcium influx into the cell via activation of slow inward calcium current

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2
Q

Function of the transverse tubules

A

Transmit electrical activity to the cell interior; located at Z-lines

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3
Q

Function of the sarcoplasmic reticulum

A

Intracellular calcium storage site

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4
Q

Function of the terminal cisternae

A

Site where calcium influx triggers opening of calcium release channels to initiate contraction

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5
Q

Longitudinal cisternae

A

Possible site of calcium reuptake to initiate relaxation

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6
Q

Function of troponin C

A

Calcium receptor on contractile protein

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7
Q

What is the difference in the contractile mechanism between cardiac and skeletal muscle?

A

There is none; they are the same

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8
Q

What is the immediate result of depolarization of T-tubules?

A

Activates calcium influx via slow inward calcium current

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9
Q

When slow inward calcium current flux is in effect, where does the calcium bind and what does it do?

A

Binds to the calcium release channels on the sarcoplasmic reticulum and opens them

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10
Q

What is the name for the SR calcium release channels?

A

Ryanodine reeptors

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11
Q

What initiates contraction of the heart muscle?

A

Calcium that is released fro the sarcoplasmic reticulum binds to troponin C

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12
Q

How long is contraction maintained?

A

As long as cytosolic calcium remains elevated

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13
Q

How is relaxation initiated?

A

Removal of cytosolic calcium by

  1. sarcoplasmic calcium uptake
  2. calcium efflux out via NCX
  3. calcium efflux out via sarcolemmal calcium pump
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14
Q

Difference in length between cardiac and skeletal cells

A

Cardiac are small (50-100 um); skeletal cells could run the whole length of the muscle

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15
Q

Difference in connectivity of cells between cardiac and skeletal

A

Cardiac cells have a syncytium that connects all the cells via gap junctions. Skeletal muscle cells are all individual

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16
Q

Difference in activation between cardiac and skeletal cells

A

Cardiac: activated by cell-to-cell conduction
Muscle: activated by neurochemical transmission at neuromuscular junctions

17
Q

Calcium dependence during contraction: cardiac vs skeletal

A

Cardiac: contraction is dependent on calcium influx (CICR)
Skeletal: Contraction is mediated by voltage sensors

18
Q

Cardiac vs skeletal: how is contraction amplitude regulated?

A

Cardiac: via slow calcium current and sarcoplasmic calcium content
Skeletal: by frequency of action potentials and central recruitment of muscle fibers

19
Q

Cardiac vs skeletal: summation

A

Cardiac: no summation or tetanus
Skeletal: summation and tetanus generates maximum tension

20
Q

Anaerobic or aerobic: cardiac vs skeletal

A

Cardiac: highly aerobic, 35% mitochondrial density
Skeletal: highly anaerobic, 2% mitochondrial density

21
Q

Are catecholamines positive or negative inotropic agents?

A

Positive

22
Q

Mechanism of catecholamines

A
  1. Binds to beta-adrenergic receptors
  2. Gs activates adenylate cyclase to increase cAMP
  3. cAMP activates cAMP-dependent protein kinase A
  4. PKA phosphorylates stuff
23
Q

What does PKA phosphorylate?

A
  1. Calcium channels to increase influx
  2. Phospholamban to increase SR calcium uptake
  3. Both #1 and #2 increase CICR
24
Q

Effectively, what are the effects of PKA phosphorylation?

A

Phospholamban phosphorylation enhances efficacy of relaxation while shortening time it takes to do so.
Increasing CICR increases contraction strength

25
Q

What is an example of a cardiac glycoside?

A

Digitalis

26
Q

Are cardiac glycosides positive or negative inotropic agents?

A

Positive

27
Q

For what pathology are cardiac glycosides prescribed?

A

Congestive heart failure

28
Q

Mechanism of cardiac glycosides

A
  1. Inhibits Na-K pump
  2. Increased intracellular [Na] decreases the [Na] gradient
  3. Calcium extrusion by NXC is reduced, increasing intracellular [Ca]
  4. Increased SR [Ca] leads to greater calcium release, and therefore, contraction
29
Q

Examples of calcium channel blockers

A

Verapamil, diltiazem, nifedipine

30
Q

For what purpose are calcium channel blockers used clinically?

A

As vasodilators and anti-arrhythmic agents

31
Q

Mechanism of calcium channel blockers

A
  1. Blocks calcium influx via calcium channels (i.e., blocks CICR)
  2. Decreased SR calcium release and SR calcium content leads to less contraction on vascular smooth muscle (vasodilation)
32
Q

Where do the anti-arrhythmic effects of calcium originate?

A

inhibition of slow inward calcium current, which inhibits conduction of AV node action potential to block SVT

33
Q

What is an unwanted side effect of calcium channel blockers?

A

Due to decrease in the CICR, it has negative inotropic effects on the heart

34
Q

Force-frequency relationship

A

Beating rate and rhythm of the heart influences cardiac contraction amplitude by altering contractility. Changes in the cycle length alter the time available for intracellular calcium handling, which alters contractility

FHB exam one (23 decks)

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