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pharm exam 2 > Topic 9 CaChannelBlockers > Flashcards

Topic 9 CaChannelBlockers Flashcards

1
Q

Most common form of angina

A

Classic Angina

The pattern of pain remains stable

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2
Q

Classic Angina caused by

A

Caused by a fixed coronary artery
obstruction (generally atheromatous)
The pattern of pain remains stable

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3
Q

Classic Angina pain relieved by what?

A

Pain is relieved by rest or nitroglycerin

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4
Q

What is Unstable Angina?

A

Pain at rest or with increasing frequency, duration, severity, or as the result of less exertion

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5
Q

Unstable angina pain not relieved by what?

A

Pain not relieved by NTG or prolonged

(>20 minutes) rest

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6
Q

Prinzmetal Angina pain?

A
  • Pain is episodic and unrelated to exertion

- Angina is the result of arteriospasm and unrelated to exertion or rest

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7
Q

Prinzmetal Angina is treated with?

A

Treated with NTG or Calcium Channel Blockers

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8
Q

Acute Coronary Syndrome

A

Atheromatous plaque ruptures
Inflammatory cells and mediators are activated
Vasoconstriction occurs

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9
Q

Acute Coronary Syndrome form what?

A

Lipid Pool
Thrombus forms and propagates
Vasoconstriction occurs

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10
Q

Acute Coronary Syndrome what biomarkers are released?

A

Characteristic MI “biomarkers” are released

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11
Q

What happens with Acute Coronary Syndrom

A

Vascular occlusion occurs

Cardiac muscle sickens and dies

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12
Q

Mixed Angina is caused by what?

A

Caused by a fixed obstruction combined

with vasospasm &/or endothelial disruptions

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13
Q

What is Mixed Angina ?

A

Patients have angina during exertion and at rest

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14
Q

Rx strategies for Angina

A

1) Increase O₂ delivery

2) Decrease O₂ demand

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15
Q

Heart extracts what % of oxygen that is delivered to them

A

extracts ~75% of oxygen delivered to it

at rest

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16
Q

What determines how much myocardial wall stress is necessary to overcome that resistance and pump blood ?

A

Arterial blood pressure

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17
Q

arterial (overwhelmingly arteriolar) tone determines what?

A

determines SVR ~~ systolic wall stress

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18
Q

Venous (capacitance) tone determines

A

how much blood can be “stored” in the
venous blood delivery system before it’s
returned to the heart

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19
Q

What determines how much blood can be “stored” in the venous blood delivery system before it’s returned to the heart

A

Venous (capacitance) tone

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20
Q

venous tone determines

A

diastolic wall stress

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21
Q

Diastolic wall stress is determined by what?

A

Venous tone

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22
Q

Organic Nitrates and Nitrites cause what? relief what?

A

Cause rapid decrease in my0 ₂cardial demand and prompt relief of stable, unstable, and variant angina

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23
Q

Nitroglycerin

A

Nitrobid

Organic Nitrates and Nitrites

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24
Q

Nitroprusside

A

Nipride

Organic Nitrates and Nitrites

25
Q

Isosorbide mononitrate

A

Imdur

Organic Nitrates and Nitrites

26
Q

Isosorbide dinitrate

A

Isordil

Organic Nitrates and Nitrites

27
Q

the most commonly used nitrate/nitrite

A

Nitroglycerin

28
Q

Organic Nitrates and Nitrites side affects

A

Cyanide toxicity and Nipride (discussed earlier)

  • Reflex tachycardia (Increase myo₂cardial demand and decrease coronary perfusion via diastolic filling)
  • Reflex positive inotropy (increase myo₂cardial demand)
29
Q

High sustained doses of Organic Nitrates and Nitrites can cause what?

A

High sustained doses can cause methemoglobinemia particularly in peds +/-Tylenol exposure

30
Q

chocolate brown blood, blood with an oxidized heme group

A

“methemoglobinemia”

31
Q

If your patient has Methemoglobinemia what are the 4 steps you take?

A 
#1) Tell the physician
#2) Prepare to give methylene blue at 1-2 mg/kg (up to 50 mg) IV over 3-5 minutes 
#3)...and ascorbic acid
#4) ...and lots of pure O2
32
Q

If a patient with Methemoglobinemia does not respond to initial typical therapy (the 4 steps) what is prob going on?

A

They are deficient in glucose-6-phosphate dehydrogenase (G6PD)

33
Q

G6PD-deficient patients who don’t respond to methylene blue and ascorbic acid require what two things?

A

1) Exchange transfusions

2) Hyperbaric oxygen

34
Q

Sodium Channel Blockers effect what?

A

Effect the transmembrane sodium/calcium exchange.

Less calcium enters the cardiomyocyte to relieve the cardiac workload

35
Q

Ranolazine

A

Ranexa

Sodium Channel Blocker

36
Q

Ranexa

A

Ranolazine

Sodium Channel Blocker

37
Q

Ranolazine (Ranexa) works by shifting what?

A

Also works by shifting cardiac metabolism from fatty acids…to carbs Which require less O₂ to metabolize

38
Q

Cardiac ischemia does what?

A

Cardiac ischemia decreases the transmembrane potential, increases the Ca⁺⁺ flow into cells which activates ATP-consuming systems which causes a positive feedback loop contributing to even more profound ischemia

39
Q

Ca Channel Blockers do what?

A

Block the calcium cardiac transmembrane current is critical in myocardial contraction
Smooth muscle is dependent on an inflow of Ca⁺⁺ to maintain ‘tone”
As those Ca⁺⁺ channels are “blocked”, those inner circular and outer longitudinal vascular smooth muscles relax

40
Q

Ca Channel Blockers affects what vasculature much more?

A

Arteries are much more affected by Ca⁺⁺ channel blockade…so arterial dilate, SVR drops, and arterial pressure falls

41
Q

Ca channel blockers do what to afterload and myocardial consumption

A

Consequently these agents DECREASE afterload (which DECREASE myO₂cardial consumption)
And dilate coronary arteries (which INCREASE myO₂cardial delivery)

42
Q

Ca Channel Blockers do what heart failure?

A

They also have the potential to worsen heart

failure

43
Q

Verapamil

A

Calan, Isoptin

Ca Channel Blockers

44
Q

Diltiazem

A

(Cardizem)

Ca Channel Blockers

45
Q

Nifedipine

A

(Procardia)

Ca Channel Blockers

46
Q

Nifedipine (Procardia) is a derivative of what?

A

dihydropyridine derivative

47
Q

Nifedipine (Procardia) has what effects?

A

Almost exclusively a vasodilator with little dromotropic or chronotropic effect.
*D.O.C. for variant angina

48
Q

Nifedipine (Procardia) causes what HR side affect?

A

Causes reflex tachycardia

49
Q

Verapamil (calan, Isoptin) is a derivative of what?

A

A diphenalkylamine derivative

50
Q

Verapamil (calan, Isoptin) causes what effects?

A

Strong negative dromotropic, chronotropic, and inotropic effects.
-Weak vasodilatory effects

51
Q

Verapamil (calan, Isoptin) does what with impulse conduction?

A

Dramatically decreases impulse conduction through the SA & AV nodes which are rich in calcium pumps.
*D.O.C. for many supraventricular tachyarrhythmias, such as SVT

52
Q

Diltiazem (Cardizem) is classified as what?

A

Classified as a benzothiazepine

53
Q

Diltiazem (Cardizem) has what effects?

A

mix of vasodilatory and cardiac effects

54
Q

Diltiazem (Cardizem) has what effects compared to verapamil? (Chonotripic, SVR, Tachycardia)

A

Less negative chronotropic and dromotropic than verapamil, less decrease SVR and reflex tachycardia than nifedipine

55
Q

What drug is utilized extensively to prevent radial artery spasm during harvest and post-operatively to maintain patency

A

Diltiazem (Cardizem) (Ca Channel Blocker)

56
Q

β- Blockers, chonotropic/inotropic effects?

A

Act as negative chronotropes and inotropes to DECREASE myO₂cardial consumption

57
Q

β- Blockers are the D.O.C. for what?

A

D.O.C. for exercise-induced angina

58
Q

Verapamil (calan, Isoptin) is the DOC for what?

A

many supraventricular tachyarrhythmias, such as SVT

59
Q

β-Blockers and Ca⁺⁺ Channel Blockers are commonly administered with what?

A

nitrates

pharm exam 2 (9 decks)

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