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Cardiology > Lecture 31: Angina and Hypertension Drugs > Flashcards

Lecture 31: Angina and Hypertension Drugs Flashcards

1
Q

Drugs used to treat angina (classes, 4)

A

Nitrates, Ca2+ channel blockers, beta blockers, late Na+ channel blocker

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2
Q

Drugs used to treat HT (classes, 7)

A

Diuretics, ACEis etc, Ca2+ channel blockers, beta blockers, alpha blockers, combo beta and alpha blockers, alpha agonists, other vasodilators

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3
Q

What is the primary goal of pharmacological treatment of angina. What three things determines this?

A

Decrease mycoardial oxygen demand (ventricular wall stress, heart rate, contractility)

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4
Q

What determines ventricular wall stress?

A

Afterload (AS/HTN), preload (volume), ventricular wall thickness

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5
Q

Three key nitrates

A

Nitrogylcerin, isosorbide dinitrate, nitroprusside

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6
Q

Nitrates: mechanism

A

Nitrates release NO –> cGMP –> dephosphorylation of myoslin light chain phosphate –> relaxation

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7
Q

What vessels do nitrates dilate? And what does this all do?

A

Veins (decrease preload) > arteries (decrease afterload, may help increase coronary flow) > arterioles (decrease afterload)

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8
Q

How can nitrates affect the HR?

A

Reflex tachycardia

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9
Q

Primary clinical indication for nitrates

A

Angina

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10
Q

What nitrate can be used in hypertensive emergency

A

Nitroprusside

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11
Q

Besides tachycardia, what other SEs do you get with nitrates?

A

Orthostatic hypotension, headache (vasodilationof meningeal artery)

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12
Q

Do not use nitrates with…why? Mechanism?

A

PDE-5 inhibitor (sildenafil) because they will cause PROFOUND hypotension; PDE inhibits cGMP –> GMP, so you get more cGMP –> MORE RELAXATION

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13
Q

Nitroprusside: PKs. What does this mean?

A

Nitroprusside can be metabolized into CN, so LT use can cause cyanide poisoning, especially with renal failure; only use until a pt is OUT OF A HYPERTENSIVE EMERGENCY

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14
Q

Prolonged nitrate use causes…How to avoid this?

A

Tolerance (tachyphylaxis); discontinue nitrate use for 8-12 hours/day

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15
Q

Two classes of Ca2+ channel blockers and associated drugs

A

Dihydropyridines (nifedipine, amlodipine); Non-dihydropyridines (dilitiazem, verapamil)

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16
Q

Ca2+ channel blockers: mechanism

A

Blocks VG L-type CA2+ channel –> less phosphorylated myosin light chain –> relaxation of SM

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17
Q

What vessels are dilated with Ca2+ channel blockers?

A

Aterioles and arteries (afterload reduction)

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18
Q

Do Ca2+ channel blockers affect preload?

A

Not really

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19
Q

Where else do Ca2+ channel blockers work?

A

Uterus, bronchi, gut

20
Q

What’s important about non-dihydropyridines

A

More potent on cardiac L-type Ca2+ channels –> decrease cardiac contractility AND decrease HR (via affect on AV/SA node)

21
Q

So, what are non-dihydropyridines heart affects?

A

Negative inotrope, dromotrope, chronotrope

22
Q

What’s important about dihydropyridines?

A

Does not decrease cardiac contractility, but does cause greater vasodilation –> reflex tachycardia

23
Q

Which dihydropyridines causes greater reflex tachycardia?

A

Nifedipine > amlodipine

24
Q

Order HR affects of Ca2+ channel blockers

A

Fast –> slow: nifedipine –> amlodipine –> verapamil, diltiazem

25
Q

Clinical indications of Ca2+ channel blockers

A

Angia, HTN, supraventricular tachycardia (for non-dihydropyridines)

26
Q

Ca2+ channel blockers: SEs

A

Hypotension, edema (decreased renal perfusion –> aldosterone), constipation (gut relaxation)

27
Q

Verapamil and diltiazem: SEs

A

Exacerbates CHF (decreae contractility), bradycardia

28
Q

Nifedipine: SEs

A

Reflex tachycardia

29
Q

Ranolazine: mechanism

A

Late Na+ current inhibitor; in ischemia causes prolonged activation of late Na+ current –> high Na+ in cell –> NCX FLIPS –> high Ca2+ in cell –> myocyte dysfunction and increased O2 demand

30
Q

Summarize the mechanism of Ranolazine and point out a cool effect

A

Keeps Ca2+ in cell NORMAL –> improves O2 consumption in ischemic cell; only effects ischemic cells!

31
Q

Primary clinical indication for ranolazine

A

Stable angina

32
Q

T/F: Does ranolazine affect BP?

A

Nope

33
Q

Ranolazine: SEs

A

Prolongs QT interval (blocks IKr)

34
Q

T/F: Ranolazine can cause torsades de pointes

A

Low risk due to balanced effect of IKr and late sodium current inhibition

35
Q

Thiazides: mechanism

A

Inhibit NaCl symporter in distal convoluted tubule

36
Q

Thiazides: SEs

A

Hypokalemia (same mechanism as furosemide), volme depletion, hypotension

37
Q

Thiazides: clinical indications (2) and one note

A

Hypertension, edema (CHF, cirrhosis, renal failure/proteinuria); note: NOT AS GOOD AT EDEMA AS FUROSEMIDE

38
Q

Other vasodilators

A

Hydralazine, minoxidil

39
Q

Hydralazine: clinical indications and important note

A

Hypertension; in combination with isosorbide dinitrate decreased mortality in African American CHF patients

40
Q

Hydralazine: SEs, including one rare one

A

Hypotension, reflex tackycardia, edema (from increased aldosterone), rare: drug-induced lupus erythematosus

41
Q

Minoxidil: mechanism

A

Opens ATP-dependent K+ channels in arterioles –> K+ exits cell –> inhibition of VG Ca2+ channel –> decreased Ca2+ –> relaxation

42
Q

Minoxidil affects what vessels?

A

Arterioles but NOT veins

43
Q

Clinical indication of minoxidil and important note

A

Hypertension, but not 1st line due to SEs

44
Q

Minoxidil: SEs

A

Hypotension, reflex tachycardia, edema (increased aldosterone), hypertrichosis

45
Q

Because of tachycardia/edema, what do you use minoxidil in combination with? (2)

A

Beta-blocker and diuretic

Cardiology (22 decks)

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