CV Flashcards

1
Q

1% increase in endo function can cause _% increase in life expectancy?

A

13%

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2
Q

list ways endothelial function can be measured

A

IVUS, laser doppler flowmetry, blood biomarkers (ICAM, VCAM, NO)

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3
Q

endothelium-derived chemicals (vasodilatory)

A

NO, PGs, endothelium-derived hyperpolarising factors

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4
Q

endothelium-derived chemicals (vasoconstricting)

A

endothelin, prostanoids

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5
Q

3 types of NOS

A

neuronal, inducible, endothelial

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6
Q

how does eNOS produce NO?

A

conversion of L-arginine and O2 into L-citrulline and NO

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7
Q

what maintains eNOS in its dimeric form?

A

BH4

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8
Q

why is BH4 necessary for eNOS function?

A

Keeps eNOS in dimeric form, if monomeric, O2 gets converted into O2- (ROS) and NO cannot be produced

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9
Q

how does NO bring about vasodilation?

A

NO in EC -> VSMC, activates sGC which catalyses cGMP -> activates PKG, which brings about vasodilatory responses

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10
Q

what does PKG do?

A

inhibits Ca release from SR, activates ca-dependent K+ channel which then inhibits LTCCs, and decreases sensitivity of myosin (reducing its phos and thus causing relaxation)

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11
Q

what management potential was highlighted in the paper

A

anti-hypertensive targeting. specifically for patients who are insensitive to dietary salt or who do not react effectively to ACEi/ARBs

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12
Q

what do the findings suggest about NSAIDS’ hypertensive SE?

A

likely brought about as a result of decreased PG production by COX inhibition, and thus reduced activation of EP4 (etc), therefore less NO produced and vasorelaxation is reduced.

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13
Q

key paper conclusions

A

EP4 activation enhances vasodilation in a NO/eNOS-dependent manner via the AMPK mechanism

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