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Pharm > Exam 2: Vasodilators/Angina > Flashcards

Exam 2: Vasodilators/Angina Flashcards

1
Q

Types of vascular tone

A

Arteriolar, capillary, venous tone

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2
Q

Describe venous tone and how it’s composition is advantageous

A

2-3 times larger than arteries. Lack of musculature allows veins to have increased capacitance

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3
Q

Blood vessel diameter relationship to resistance of vessel

A

The larger the diameter the less the resistance.

Doubling the diameter has resulting in 1/16 of the initial resistance. Larger diameter greater flow. Doubling the diameter increased flow by 16 times.

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4
Q

Steps in Blood vessel contraction

A

Contraction thru trigger calcium influx. Calcium binds to calmodulin (calcium modulator).
Ca and calmodulin activate MLCK. MLCK attaches Phosphate to Myosin light chain. MLC causes contraction.

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5
Q

What blocks MLCK from activating MLC

A

cAMP causes a phosphorylation cascade. MLCK is inactivated when phosphorylated. Therefore cAMP blocks contraction of blood vessels.

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6
Q

Venous system functions

A

Return blood to heart and acts as reservoir for blood volume (veins contain 70% of blood volume).

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7
Q

Angina pectoris definition

A

Chest pain

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8
Q

Hearts preferred source of energy

A

Fatty acid oxidation

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9
Q

Classic angina is also referred to as

A

Angina of effort

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10
Q

List causes of variant angina

A

Coronary vasospasm
Aka Vasospastic
Aka prinzmetal angina

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11
Q

Unstable angina is also referred to

A

Angina at rest

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12
Q

Which form of angina is a medical emergency

A

Unstable angina/angina at rest aka Acute coronary syndrome.

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13
Q

Treatment for classic angina

A

Reduction of demand.
Meds: can give nitro

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14
Q

Treatment for variant angina

A

Potent vasodilators, nitrates. Calcium ch blockers can be given prophylactically.

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15
Q

Coronary Blood Flow is Inversely proportional to

A

coronary vascular bed resistance

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16
Q

Coronary blood flow is directly related to what

A

Perfusion pressure and duration of diastole.

17
Q

Myosin light chains active and inactive forms

A

Myosin light chains are activated when phosphorylated.
MLC are inactive without this phosphorylation

18
Q

Myosin light chain kinase active and inactive forms

A

MLCK is active when it is not phosphorylated.
MLCK is inactive when it is phosphorylated.

19
Q

What inactivates MLCK

A

cAMP. cAMP causes phosphorylation cascade.

20
Q

What activates or phosphorylates MLC

A

MLCK

21
Q

Nitrates/nitrites impact of vasculature

A

Increases venous capacitance of large veins. Also decreases force, and wall stress which improves myocyte perfusion. This is the drugs best response.

Large arteries will dilate with large doses.

22
Q

Nitric oxide activates guanylyl cyclase which activates cGMP. What is cGMPs role in reducing contraction

A

cGMP strips PO4 from MLC rendering it inactive, leading to relaxation.

23
Q

What breaks down cGMP

A

PDE- phospodiesterase

24
Q

How can we prolong cGMP, thereby increasing duration of relaxation?

A

PDE can be blocked thru phosphodiesterase inhibitors. This prolongs cGMP presence therefore prolonging relaxation.

25
Q

Nitrates/nitrites The Good

A

Increased venous capacitance, decreased preload, decreased CO, decreased heart size.

26
Q

Nitrates/nitrites: The Bad
Minor Side effects

A

Orthostatic hypotension, syncope, Headache.

27
Q

Nitrates/nitrites The Ugly

A

Reflex tachycardia and HgB interactions.

28
Q

nitrite ions interact with HgB to form what

A

Methemoglobin

29
Q

Downside of methemoglobin

A

Low affinity for oxygen

30
Q

Benefit of methemoglobin

A

Very High affinity for cyanide. Can be given in excess to help clear cyanide

31
Q

How does cAMPs role differ in heart vs vasculature

A

cAMP increases force and rate of contraction in the heart.
cAMP inhibits MLCK from activating MLC and causes relaxation in vasculature.

32
Q

What are pFOX inhibitors and what is there role in cardiac metabolism

A

Heart prefers fatty acid for energy. pFOX inhibitors decrease fatty acid oxidation and increase glucose use of the heart. This is a more efficient form of energy (glucose).
Being efficient it decreases O2 requirements in cardiac metabolism.

33
Q

What are pFOX inhibitors and what is there role in cardiac metabolism

A

Heart prefers fatty acid for energy. pFOX inhibitors decrease fatty acid oxidation and increase glucose use of the heart. This is a more efficient form of energy (glucose).
Being efficient it decreases O2 requirements in cardiac metabolism.

34
Q

Contraindicated vasodilators for Angina

A

Hydralazine and minoxidil. Increase SNS input, may increase angina.

Sodium Nitroprusside- higher toxicity, better agents for angina.

Fenoldepam- reflex tachycardia

35
Q

Non pharmaceutical Interventions for angina: (procedures)

A

CABG, cardiac cath, stent

Pharm (8 decks)

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