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Regulation of Blood Flow Flashcards

1
Q

Acebutolol

A

Beta 1 antagonist (selective)

Decrease heart rate and contractility
• Decrease renin release

Adverse effects
– Bronchospasm (avoid in asthmatics)
– Poor outcomes: increase Type 2 diabetes
– Hypoglycemia, hyperlipidemia
– Myocardial depression, bradycardia, reduced
exercise tolerance
– Sleep disturbances, cold extremities
– Impotence
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2
Q

atenolol

A

Beta 1 antagonist (selective)

Decrease heart rate and contractility
• Decrease renin release

Adverse effects
– Bronchospasm (avoid in asthmatics)
– Poor outcomes: increase Type 2 diabetes
– Hypoglycemia, hyperlipidemia
– Myocardial depression, bradycardia, reduced
exercise tolerance
– Sleep disturbances, cold extremities
– Impotence
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3
Q

esmolol

A

Beta 1 antagonist (selective)

Decrease heart rate and contractility
• Decrease renin release

Adverse effects
– Bronchospasm (avoid in asthmatics)
– Poor outcomes: increase Type 2 diabetes
– Hypoglycemia, hyperlipidemia
– Myocardial depression, bradycardia, reduced
exercise tolerance
– Sleep disturbances, cold extremities
– Impotence
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4
Q

metoprolol

A

Beta 1 antagonist (selective)

Decrease heart rate and contractility
• Decrease renin release

Adverse effects
– Bronchospasm (avoid in asthmatics)
– Poor outcomes: increase Type 2 diabetes
– Hypoglycemia, hyperlipidemia
– Myocardial depression, bradycardia, reduced
exercise tolerance
– Sleep disturbances, cold extremities
– Impotence
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5
Q

nadolol

A

beta antagonist (non-selective)

Decrease heart rate and contractility
• Decrease renin release
• Potentiate

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6
Q

pindolol

A

beta antagonist (non-selective)

ISA=intrinsic sympathomimetic activity (partial agonist)

Decrease heart rate and contractility
• Decrease renin release
• Potentiate

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7
Q

propranolol

A

beta antagonist (non-selective)

Decrease heart rate and contractility
• Decrease renin release
• Potentiate

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8
Q

timolol

A

beta antagonist (non-selective)

Decrease heart rate and contractility
• Decrease renin release
• Potentiate

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9
Q

avanafil

A

PDE5 inhibitor

– Increase levels of cGMP
– Modest drop in blood pressure

Combo with nitrates or

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10
Q

sildenafil

A

PDE5 inhibitor

– Increase levels of cGMP
– Modest drop in blood pressure

Combo with nitrates or

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11
Q

tadalafil

A

PDE5 inhibitor

– Increase levels of cGMP
– Modest drop in blood pressure

Combo with nitrates or

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12
Q

vardenanfil

A

PDE5 inhibitor

– Increase levels of cGMP
– Modest drop in blood pressure

Combo with nitrates or

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13
Q

dilitiazem

A

Ca channel blocker (cardioselective)

Block voltage dependent (L-type) Ca2+
channels
• Decrease cytosolic Ca2+

Reduce O2 demand
– Decrease arterial pressure
– Decrease contractility-verapamil
– Decrease heart rate-diltiazem and verapamil
• Increase O2 supply
– Dilate epicardial arteries and stenoses
increasing coronary blood flow
– Prevent vasospasm-coronary and cerebral
Uses
– Coronary heart disease-chronic treatment
– Hypertension
– Supraventricular arrhythmias
– Cerebral hemorrhage or vasospasm
• Less effective for secondary prevention
after MI than

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14
Q

verapamil

A

Ca channel blocker (cardioselective)

Block voltage dependent (L-type) Ca2+
channels
• Decrease cytosolic Ca2+

Reduce O2 demand
– Decrease arterial pressure
– Decrease contractility-verapamil
– Decrease heart rate-diltiazem and verapamil
• Increase O2 supply
– Dilate epicardial arteries and stenoses
increasing coronary blood flow
– Prevent vasospasm-coronary and cerebral

Uses
– Coronary heart disease-chronic treatment
– Hypertension
– Supraventricular arrhythmias
– Cerebral hemorrhage or vasospasm
• Less effective for secondary prevention
after MI than

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15
Q

amlodipine

A

Ca channel blocker (vasoselective)

Block voltage dependent (L-type) Ca2+
channels
• Decrease cytosolic Ca2+

Reduce O2 demand
– Decrease arterial pressure
– Decrease contractility-verapamil
– Decrease heart rate-diltiazem and verapamil
• Increase O2 supply
– Dilate epicardial arteries and stenoses
increasing coronary blood flow
– Prevent vasospasm-coronary and cerebral

Uses
– Coronary heart disease-chronic treatment
– Hypertension
– Supraventricular arrhythmias
– Cerebral hemorrhage or vasospasm
• Less effective for secondary prevention
after MI than

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16
Q

nicardipine

A

Ca channel blocker (vasoselective)

Block voltage dependent (L-type) Ca2+
channels
• Decrease cytosolic Ca2+

Reduce O2 demand
– Decrease arterial pressure
– Decrease contractility-verapamil
– Decrease heart rate-diltiazem and verapamil
• Increase O2 supply
– Dilate epicardial arteries and stenoses
increasing coronary blood flow
– Prevent vasospasm-coronary and cerebral

Uses
– Coronary heart disease-chronic treatment
– Hypertension
– Supraventricular arrhythmias
– Cerebral hemorrhage or vasospasm
• Less effective for secondary prevention
after MI than

17
Q

nifedipine

A

Ca channel blocker (vasoselective)

Block voltage dependent (L-type) Ca2+
channels
• Decrease cytosolic Ca2+

Reduce O2 demand
– Decrease arterial pressure
– Decrease contractility-verapamil
– Decrease heart rate-diltiazem and verapamil
• Increase O2 supply
– Dilate epicardial arteries and stenoses
increasing coronary blood flow
– Prevent vasospasm-coronary and cerebral

Uses
– Coronary heart disease-chronic treatment
– Hypertension
– Supraventricular arrhythmias
– Cerebral hemorrhage or vasospasm
• Less effective for secondary prevention
after MI than

18
Q

nimodipine

A

Ca channel blocker (vasoselective)

Nimodipine (Nimotop®) used in subarachnoid
hemorrhage only-more lipophilic

Block voltage dependent (L-type) Ca2+
channels
• Decrease cytosolic Ca2+

Reduce O2 demand
– Decrease arterial pressure
– Decrease contractility-verapamil
– Decrease heart rate-diltiazem and verapamil
• Increase O2 supply
– Dilate epicardial arteries and stenoses
increasing coronary blood flow
– Prevent vasospasm-coronary and cerebral
Peripheral edema

19
Q

isosorbide dinitrate

A

Nitrovasodilator

Activated by p450

Reduce O2 demand
– Venodilator
decrease preload
– Arterial vasodilator
decrease afterload
– Reduce wall stress
and MVO2
– Indirect reflex
increase in heart rate
and contractility
• Increase O2 supply
– Dilate conduit arteries
esp. at stenosis
– Increase collateral blood
flow
– Increase subendocardial
blood flow
– Decreased platelet
activation
  • Relaxes large arteries (relief of vasospasm)
  • Relaxes veins (decrease LV filling= preload)
  • Inhibition of platelet aggregation

– Duration of action-3-5 hours
– Administered 3-4 times daily

• Nitrate tolerance:
– Decreased response, interrupt therapy 8-12 hours
• Mechanism: unclear at cellular level
– Neurohumoral counter-regulation
– Increased response to vasoconstrictors
– Impaired endothelial function
• Side/adverse effects:
– Headache: GTN>ISDN>ISMN
– Orthostatic hypotension, dizziness, flushing, syncope
– Reflex tachycardia
– GI distress (oral) or skin irritation (patch)
– Contraindicated: phosphodiesterase Type 5 (PDE5)
inhibitors

Side/adverse effects:
– Hypotension when combined with
nitrovasodilators and

20
Q

isosorbide mononitrate

A

Nitrovasodilator

Metabolized by p450

Reduce O2 demand
– Venodilator
decrease preload
– Arterial vasodilator
decrease afterload
– Reduce wall stress
and MVO2
– Indirect reflex
increase in heart rate
and contractility
• Increase O2 supply
– Dilate conduit arteries
esp. at stenosis
– Increase collateral blood
flow
– Increase subendocardial
blood flow
– Decreased platelet
activation
  • Relaxes large arteries (relief of vasospasm)
  • Relaxes veins (decrease LV filling= preload)
  • Inhibition of platelet aggregation

– Longer duration of action
– Minimal first pass metabolism

• Nitrate tolerance:
– Decreased response, interrupt therapy 8-12 hours
• Mechanism: unclear at cellular level
– Neurohumoral counter-regulation
– Increased response to vasoconstrictors
– Impaired endothelial function
• Side/adverse effects:
– Headache: GTN>ISDN>ISMN
– Orthostatic hypotension, dizziness, flushing, syncope
– Reflex tachycardia
– GI distress (oral) or skin irritation (patch)
– Contraindicated: phosphodiesterase Type 5 (PDE5)
inhibitors

Side/adverse effects:
– Hypotension when combined with
nitrovasodilators and

21
Q

nitroglycerin

A

Nitrovasodilator (GTN)

Activated by mito Aldehyde Dehydrogenase

Reduce O2 demand
– Venodilator
decrease preload
– Arterial vasodilator
decrease afterload
– Reduce wall stress
and MVO2
– Indirect reflex
increase in heart rate
and contractility
• Increase O2 supply
– Dilate conduit arteries
esp. at stenosis
– Increase collateral blood
flow
– Increase subendocardial
blood flow
– Decreased platelet
activation
  • Relaxes large arteries (relief of vasospasm)
  • Relaxes veins (decrease LV filling= preload)
  • Inhibition of platelet aggregation

– First pass hepatic metabolism
– Duration of action-dependent on formulation

• Nitrate tolerance:
– Decreased response, interrupt therapy 8-12 hours
• Mechanism: unclear at cellular level
– Neurohumoral counter-regulation
– Increased response to vasoconstrictors
– Impaired endothelial function
• Side/adverse effects:
– Headache: GTN>ISDN>ISMN
– Orthostatic hypotension, dizziness, flushing, syncope
– Reflex tachycardia
– GI distress (oral) or skin irritation (patch)
– Contraindicated: phosphodiesterase Type 5 (PDE5)
inhibitors

Side/adverse effects:
– Hypotension when combined with
nitrovasodilators and

22
Q

nitroprusside sodium

A

Nitrovasodilator

Straight to NO

Reduce O2 demand
– Venodilator
decrease preload
– Arterial vasodilator
decrease afterload
– Reduce wall stress
and MVO2
– Indirect reflex
increase in heart rate
and contractility
• Increase O2 supply
– Dilate conduit arteries
esp. at stenosis
– Increase collateral blood
flow
– Increase subendocardial
blood flow
– Decreased platelet
activation
  • Relaxes large arteries (relief of vasospasm)
  • Relaxes veins (decrease LV filling= preload)
  • Inhibition of platelet aggregation

• Nitrate tolerance:
– Decreased response, interrupt therapy 8-12 hours
• Mechanism: unclear at cellular level
– Neurohumoral counter-regulation
– Increased response to vasoconstrictors
– Impaired endothelial function
• Side/adverse effects:
– Headache: GTN>ISDN>ISMN
– Orthostatic hypotension, dizziness, flushing, syncope
– Reflex tachycardia
– GI distress (oral) or skin irritation (patch)
– Contraindicated: phosphodiesterase Type 5 (PDE5)
inhibitors

Side/adverse effects:
– Hypotension when combined with
nitrovasodilators and

23
Q

Asprin

A

misc. blood flow regulator

non-selective cyclooxygenase inhibitor

part of MONO
- Morphine, Oxygen, Nitroglycerin, Aspirin

24
Q

clopidogrel

A

misc. blood flow regulator

Platelet P2Y12 inhibitors

Mechanism of action
– Different hepatic biotransformation pathways
– ADP antagonists at P2Y12 receptor
– Block ADP-mediated activation of glycoprotein GPIIb/IIIa
– Prevent platelet aggregation
• Use: in combination with aspirin in ACS (esp.
stents), MI and stroke
• Adverse effect: neutropenia with clopidogrel
– Genetic variability in clopidogrel metabolism
– Prasugrel: fewest drug interactions

Hepatic Metabolism: CYP2C19

Low metabolic activation (15%)
85% inactive metabolite

25
Q

prasugrel

A

misc. blood flow regulator

Platelet P2Y12 inhibitors

Mechanism of action
– Different hepatic biotransformation pathways
– ADP antagonists at P2Y12 receptor
– Block ADP-mediated activation of glycoprotein GPIIb/IIIa
– Prevent platelet aggregation
• Use: in combination with aspirin in ACS (esp.
stents), MI and stroke
• Adverse effect: neutropenia with clopidogrel
– Genetic variability in clopidogrel metabolism
– Prasugrel: fewest drug interactions

Rapid 100% GI absorption
Not metabolized by CYP2C19
100% metabolic activation

26
Q

ranolazine

A

misc. blood flow regulator

First new class of antianginal in 20 years
– Approved for use in US 2006
• Piperazine derivative
– Partial fatty-acid oxidation (PFox) inhibitor
• Mechanism of action
– Inhibits late sodium current to reduce [Na+]i
and Ca2+ overload in ischemic myocytes

27
Q

ticagrelor

A

misc. blood flow regulator

Platelet P2Y12 inhibitors
Non-thienopyridine

Mechanism of action
– Different hepatic biotransformation pathways
– ADP antagonists at P2Y12 receptor
– Block ADP-mediated activation of glycoprotein GPIIb/IIIa
– Prevent platelet aggregation
• Use: in combination with aspirin in ACS (esp.
stents), MI and stroke
• Adverse effect: neutropenia with clopidogrel
– Genetic variability in clopidogrel metabolism
– Prasugrel: fewest drug interactions

Active parent
Not metabolized via CYP2C19

Pharma (39 decks)

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