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Pharm Exam 2 > Topic 9 > Flashcards

Topic 9 Flashcards

1
Q

4 calcium channel blocker categories

A

Organic Nitrates
Sodium Channel Blockers
Calcium Channel Blockers
β-Blockers

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2
Q

5 types of angina

A

1) “Classic”, “Stable”, or “Effort-Induced”
2) “Unstable”
3) “Variant”, “Rest”, “Vasospastic”, or “Prinzmetal”
4) “Acute Coronary Syndrome”
5) “Mixed”

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3
Q

Most common type of angina

A

Classic

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4
Q

Classic angina is caused by

A

a fixed coronary artery obstruction

generally atheromatous

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5
Q

With classic angina, the pattern of pain remains

A

stable

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6
Q

With classic angina, the pain is relieved by

A

rest or nitroglycerin

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7
Q

Unstable angina=

A

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

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8
Q

With unstable angina, pain is

A

not relieved by NTG or prolonged (>20 minutes) rest

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9
Q

With Prinzmetal angina, pain is

A

episodic and unrelated to exertion

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10
Q

Prinzmetal angina: Although patient might have

atherosclerosis, angina is the result of

A

arteriospasm and unrelated to exertion or rest

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11
Q

Treat Prinzmetal angina with

A

NTG

Calcium Channel Blockers

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12
Q

Acute coronary syndrome=

A
  • Atheromatous plaque ruptures
  • Inflammatory cells and mediators are activated
  • “Lipid Pool” forms
  • Thrombus forms and propagates
  • Vasoconstriction occurs
  • Vascular occlusion occurs
  • Cardiac muscle sickens and dies
  • Characteristic MI “biomarkers” are released
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13
Q

Mixed angina=

A
  • Patients have angina during exertion and at rest.

- Caused by a fixed obstruction combined with vasospasm &/or endothelial disruptions

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14
Q

Angina treatment strategies include

A

Increase O₂ delivery

Decrease O₂ demand

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15
Q

Determinants of myocardial O2 consumption

A
  1. Wall stress (Intraventricular pressure, Ventricular radius/volume, Wall thickness)
  2. Heart rate
  3. Contractility
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16
Q

The heart extracts ___% of oxygen delivered to it

at rest.

A

75%

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17
Q

Arterial blood pressure determines how

much

A

myocardial wall stress is necessary to overcome that resistance and pump blood

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18
Q

arterial (overwhelmingly arteriolar) tone determines

A

SVR ~~ systolic wall stress

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19
Q

Venous (capacitance) tone determines

A

~~diastolic wall stress.

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

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20
Q

Organic Nitrates and Nitrites causes

A

rapid decrease in my0₂cardial demand and prompt relief of stable, unstable, and variant angina

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21
Q

Organic Nitrates and Nitrites all work similarly and differ in their

A

onset and duration of action

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22
Q

Organic Nitrates and Nitrites include (4)

A

Nitroglycerin (Nitrobid)
Nitroprusside (Nipride)
Isosorbide mononitrate (Imdur)
Isosorbide dinitrate (Isordil)

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23
Q

Nitroglycerin

A

Nitrobid

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24
Q

Nitroprusside

A

Nipride

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25
Q

Isosorbide mononitrate

A

Imdur

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26
Q

Isosorbide dinitrate

A

Isordil

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27
Q

most commonly used nitrate/nitrite and one you will become most comfy with is…

A

Nitroglycerin

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28
Q 
Organic Nitrates and Nitrites
Side Effects (3)
A

*Cyanide toxicity and Nipride
*Reflex tachycardia (myo₂ cardial demand and coronary perfusion via diastolic filling)
* Reflex positive inotropy (myo₂cardial
demand)

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29
Q

Organic Nitrates and Nitrites

High sustained doses can cause

A

methemoglobinemia

-particularly in peds exposed to Tylenol exposure

30
Q

methemoglobinemia=

A

blood with an oxidized heme group

Chocolate brown blood

31
Q

methemoglobinemia treatment

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

methemoglobinemia patient that is unresponsive treatment

A

they may be deficient in the enzyme glucose-6-phosphate dehydrogenase (G6PD)

33
Q

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

A

1) Exchange transfusions

2) Hyperbaric oxygen

34
Q

Sodium channel blockers=

A
  • Effect the transmembrane sodium/calcium exchange.

- Less calcium enters the cardiomyocyte to relieve the cardiac workload

35
Q

Sodium channel blocker drug name

A

Ranolazine (Ranexa)

36
Q

Ranolazine

A

Ranexa

37
Q

Sodium channel blockers act by

A

shifting cardiac metabolism from fatty acids…to carbs

-Which require less O₂ to metabolize

38
Q

The calcium cardiac transmembrane current is critical in

A

myocardial contraction

39
Q

Cardiac ischemia decreases the transmembrane

potential….. then…

A

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

40
Q

Calcium channel blockers can worsen

A

heart failure

41
Q

Smooth muscle is dependent on an inflow of

A

Ca++ to maintain tone

42
Q

As those Ca⁺⁺ channels are “blocked”…

A

inner circular and outer longitudinal vascular smooth

muscles relax.

43
Q

Arteries are much more affected by Ca⁺⁺ channel blockade, which causes

A

arterial dilate, SVR drops, and arterial pressure falls

44
Q

Calcium channel blockers do what to afterload and O2 consumption/delivery

A

decreases afterload= decreases myO₂ cardial consumption
dilate coronary arteries= increases myO₂cardial
delivery)

45
Q

Calcium channel blockers have the potential to worsen heart failure because

A
  • does not allow the heart to complete action potential- heart depolarizes but cannot re polarize
46
Q

Calcium Channel Blockers drugs

A

Verapamil (Calan, Isoptin)
Diltiazem (Cardizem)
Nifedipine (Procardia)

47
Q

Verapamil

A

(Calan, Isoptin)

48
Q

Diltiazem

A

(Cardizem)

49
Q

Nifedipine

A

(Procardia)

50
Q

Calcium channel blockers are are differentiated by their

A

ability to affect the myocardium vs. vascular smooth muscle

51
Q

Nifedipine is a derivative of

A

dihydropyridine

52
Q

Nifedipine is almost exclusively a

A

vasodilator with little dromotropic or chronotropic effect

53
Q

Nifedipine- D.O.C. for

A

variant angina

54
Q

Nifedipine Causes reflex

A

tachycardia

55
Q

Verapamil is a derivative of

A

diphenalkylamine

56
Q

Verapamil effects

A

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

57
Q

Verapamil Dramatically decreases impulse conduction through the

A

SA & AV nodes

-which are rich in calcium pumps

58
Q

Verapamil- D.O.C. for

A

many supraventricular tachyarrhythmias, such as SVT

59
Q

Diltiazem Classified as a

A

benzothiazepine

60
Q

Diltiazem has a mixture of

A

vasodilatory and cardiac effects

61
Q

Diltiazem is less____ than verapamil

A

Less negative chronotropic and dromotropic

62
Q

Diltiazem is less _____ than nifedipine

A

less decrease in SVR and reflex tachycardia

63
Q

Diltiazem is Utilized extensively to prevent

A

radial artery spasm during harvest and post-operatively to maintain patency

64
Q

β- Blockers act as

A

negative chronotropes and inotropes to decrease myO₂cardial consumption

65
Q

β- Blockers DOC

A

for exercise induced angina

66
Q

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

A

nitrates

67
Q

Drugs commonly used for treating angina with:

Concomitant disease: None

A

Long acting nitrate
B-Blockers
Ca-Blockers

68
Q

Drugs commonly used for treating angina with:

Concomitant disease: Recent MI

A

Long acting nitrate

B-Blockers

69
Q

Drugs commonly used for treating angina with:

Concomitant disease: Asthma, COPD

A

Long acting nitrate

Ca-Blockers

70
Q

Drugs commonly used for treating angina with:

Concomitant disease: HTN

A

Long acting nitrate (less effective)
B-Blockers
Ca-Blockers

71
Q

Drugs commonly used for treating angina with:

Concomitant disease: Diabetes

A

Long acting nitrate

Ca-Blockers

72
Q

Drugs commonly used for treating angina with:

Concomitant disease: Chronic renal disease

A

Long acting nitrate
B-Blockers (less effective)
Ca-Blockers

Pharm Exam 2 (9 decks)

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