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Therapeutics Spring 2016 > Exam 1 > Flashcards

Exam 1 Flashcards

1
Q

What are 9 risk factors for CAD?

A

Immediate family history of CAD, hypertension, dyslipidemia, Low HDL-c, obesity, DM, physical inactivity, stress, smoking/tobacco use

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2
Q

How do you know if someone has stable angina or not?

A

It is stable if it is relieved by either nitroglycerin or rest, and if there is an ST depression on the EKG.
It is stable if characteristics of an angina episode have not changed over 2 months.

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3
Q

What is the difference between NSTEMI and STEMI?

A

STEMI is ST wave elevation MI and is more severe than NSTEMI, which in non ST elevation MI.

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4
Q

What 5 clinical syndromes are associated with angina, but have reversible ischemia? (no tissue death)

A

Silent ischemia, stable angina pectoris, cardiac syndrome X, variant or Prinzmetal’s angina, and unstable angina.

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5
Q

When treating angina, do we use drugs to treat the oxygen demand or supply side?

A

Oxygen supply

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6
Q

What is Myocardial Ischemia?

A

It is the pathophysiological state secondary to increased myocardial work and/or decreased oxygen supply. Creates myocardial disturbances without causing necrosis.

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7
Q

What is Angina?

A

Resulting symptoms from angina and is a clinical syndrome of chest discomfort.

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8
Q

Is it possible to have ischemia without angina?

A

Yes, it is called silent ischemia

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9
Q

What 4 blood vessels are most commonly affected by CAD?

A

Right coronary artery, Left main coronary artery (Widows artery), left anterior descending artery, circumflex artery (LCX)

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10
Q

What is an atherosclerotic plaque and how can it start out as stable angina and progress to Acute Coronary Syndrome?

A

It is a lipid core surrounded by an endothelial fibrous cap that forms across an artery. It becomes unstable when the fibrous cap beaks and platelets begin adhering to the area.

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11
Q

How is Significant CAD defined?

A

> 75% atherosclerotic reduction in a major epicardial coronary vessel. About 85% of patients with angina pectoris have this.

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12
Q

What do the PQRST stand for in clinical presentation of Angina?

A

P = Precipitating factors and palliative measures
Q = Quality of pain
R = Region and radiation
S = Severity of the pain
Timing and temporal pattern (time of day)

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13
Q

Diabetic patients often have what type of CAD?

A

silent ischemia

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14
Q

What is the only definitive test for IHD?

A

Cardiac catheterization and coronary angiography.

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15
Q

What are the desired outcomes for treatment of CAD?

A

Prevent ACS and death, alleviate acute sxs and prevent recurrent sxs of ischemia and avoid/minimize adverse treatment effects.

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16
Q

What is meant by secondary prevention of CAD?

A

Modifying existing CV risk factors, slow the progression of CAS and stabilize existing AS plaques.

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17
Q

What are the A-B-C-D-E of stable angina in the guidelines?

A 
A = Aspirin, Antiplatelets,anti-anginals(these don't prevent ACS and death)
B = Beta blocker and blood pressure
C = Cholesterol and cigarettes
D = Diet and Diabetes
E = Education and Exercise
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18
Q

What class of HTN medications must be considered for all post MI patients?

A

Beta blockers

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19
Q

What 4 classes of pharmacotherapy are to prevent ACS and death?

A

Anti platelet therapy, Statin therapy, ACE inhibitor/ARB therapy, and Beta Blockers

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20
Q

Why are anti platelet medications used to prevent CAD?

A

To prevent aggregation of platelets around plaques. Can use Aspirin and an adenosine diphosphate inhibitor bc they work via two different mechanisms.

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21
Q

What is a common dose of Aspirin for Anti-platelet therapy?

A

75-162mg daily

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22
Q

What is a common dose of Clopidogrel (Plavix)

A

75mg Daily

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23
Q

What is a common dose of Prasugrel (Effient)

A

10 mg Daily

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24
Q

What is a common dose of Ticagrelor (Brilanta)

A

90mg BID

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25
Q

What is a common dose of Cangrelor (Kengreal)

A

IV ONLY, no dose given

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26
Q

Which PGY12 Inhibitor is in the cyclopentyl-triazole-pyrimidine class?

A

Ticagrelor

Clopidogrel and Prasugrel are in the Thienopyridine Class

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27
Q

How is the pharmacology different between Ticagrelor

Clopidogrel and Prasugrel?

A

Clopidegrel is CYP dependent to become active and is less potent than the other two. Prasugrel is less Cyp dependent to become active and Ticagrelor is direct acting but the Prasugrel and Ticagrelor are equally potent.

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28
Q

What is the time to peak for each of the PGY12 inhibitors?

A

All are 2-4 hours to peak, clopidegrel is dose dependent. At 300mg it takes 4-5 hours to peak, at 600mg it takes 2-3 hours to peak.

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29
Q

How much time is required for drug dissipation for the PGY12 inhibitors?

A

Clopidogrel and Ticagrelor are 5 days, Pasugrel is 7 days.

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30
Q

What are three adverse effects of Aspirin?

A

GI bleeding, Intra and extracranial bleeding and hypersensitivity. Must weigh risk vs. benefit

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31
Q

What are the adverse effects of PGY12 Inhibitors?

A

GI bleeding, diarrhea, nausea, dyspepsia(Ticagrelor greater), anorexia
Derm: Rash, pruritus, urticarial, Ecchymoses
Hematologic: Bleeding, neutropenia (clopidogrel?), aplastic anemia, TTP, thrombocytopenia
Cholestasis, hepatitis,

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32
Q

Is angina a result of increased oxygen consumption or decreased blood flow?

A

Angina pain can come from either increased oxygen consumption or decreased coronary blood flow

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33
Q

What are 3 causes of decreased coronary blood flow?

A

Vasospasms, thrombus or fixed stenosis

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34
Q

What are 4 causes of increased oxygen consumption?

A

Increased heart rate, contractilty, after load and preload

35
Q

What vessels are important to deliver blood and oxygen to the myocardium?

A

Coronary arteries

36
Q

What is preload?

A

Left ventricular end diastolic pressure or volume. This is the amount of stretch on the heart at the end of diastolic before contraction

37
Q

How is preload decreased and what does this lead to?

A

Decreased by dilation of veins. This leads to decrease in o2 consumption and increased myocardial perfusion

38
Q

How is after load defined?

A

Force that the ventricle has to push against to eject blood during systole

39
Q

How is after load decreased? What does this do to oxygen consumption?

A

Decreased by dilation of artery, leads to decreased oxygen consumption.

40
Q

What is heart rate?

A

Number of beats per minute

41
Q

When the heart rate is decreased, what effect does it have on the workload and perfusion?

A

decreases the workload and increased coronary perfusion

42
Q

What is the process of atherosclerosis formation?

A

LDL accumulates in the subendothelial region and is oxidized. This triggers various responses of the immune system including monocyte infiltration and macrophage activation. When the LDL is oxidized, this triggers signaling responses that cause uptake into macrophages, foam cell formation and fatty streak embellishment. The oxidized LDL’s also cause migration of SMC, which then proliferate, lay down collagen and other matrix components to form the lesion. A cap is then formed over this, and a rupture in this is what causes thrombosis.

43
Q

What are the 3 types of angina and are they supply or demand ischemia?

A 
Prinzmetals variant angina (vasospasm) = supply ischemia
Chronic stable angina (fixed stenosis) = demand ischemia
Unstable angina (thrombus) = supply ischemia
44
Q

What is Printzmetal’s variant angina?

A

it is a sudden transient constriction of the large coronary arteries, often occurring at night or at rest. Can also be caused by atherosclerosis due to damaged endothelium causing a narrowing.

45
Q

How is stable angina different from unstable

A

Stable: predictable, usually on exertion, after eating or due to heightened emotional states.
Unstable: Emergency type pt needs to get to hospital ASAP due to impending heart attack. Usually due to a plaque rupture followed by a clot formation in a coronary artery.

46
Q

What type of angina is most common in women and young women?

A

Pritzmetals angina/vasospastic/variant - not due to atherosclerosis itself

47
Q

What are two classes of drugs used to increase oxygen delivery to treat Angina?

A

Vasodilators: Calcium channel blockers and nitrodilaters

Antithrombotic drugs: Anti coags and anti-platelets

48
Q

What 2 drug classes are used to decrease oxygen demand to treat angina?

A

Vasodilators (via afterload and preload)

Cardiac depressants: Beta blockers, Calcium channel blockers, HCN channel inhibitors

49
Q

What drug is used to improve mechanical dysfunction, but is only a second or third line drug usually reserved for patients that cannot undergo corrective procedures?

A

Ranolazine (Should be used in combo with amlodipine, beta blockers or nitrates)

50
Q

What are adverse effects associated with Ranolazine?

A

Constipation, nausea, dizziness and headache. Dose related increase in QT-interval

51
Q

What are the 3 treatment goals highlighted by Dr Drenan for any type of angina?

A

Dilate coronary arteries, decrease oxygen demand, decrease preload and afterload

52
Q

What is the mechanism of action of organic nitrates?

A

They are nitric oxide donors/releasers that lead to the activation of guanylate cyclase causing relaxation of smooth muscles, causing an improvement in the delivery of oxygenated blood.
Main effect is to decrease preload, but does have some action on afterload and platelet aggregation.

53
Q

Which of the following organic Nitrates has the longest half life? What is the half life for each? Glyceryl trinitrate, isosorbide mononitrate, isosorbide dinitrate

A

Glyceryl trinitrate = 3 minutes
isosorbide mononitrate = 10 minutes
isosorbide dinitrate = 280minutes
The two isosorbides can be used as prevention, just need at least 8 hours between doses to prevent tolerance.

54
Q

What is the mechanism behind building a tolerance to nitrates?

A

ALDH2 is required for bioactivation of nitrates. When these medications are taken consistently there is not a sufficient amount of ALDH2 to activate the nitrates, so the drug becomes ineffective.

55
Q

What is the mechanism by which Calcium channel blockers help prevent angina?

A

These drugs decrease influx of trigger calcium in the myocytes and decrease chronotropy in nodal cells. They cause dilation of arteries, so main effect is on afterload.

56
Q

True or False: Dihydropyridine calcium channel blockers and non dihydropyridine calcium channel blockers work the same way to prevent angina.

A

False: DHP’s increase HR, have either no or a decreased effect on myocardial contractility, significant decrease in systolic pressure and little to no effect on LV volume.
Non DHP’s decrease HR (verapamil more than Diltiazem), decrease myocardial contractility and only slightly decrease systolic pressure, have the same effect on LV volume as DHP’s.

57
Q

What two drugs commonly used for Angina prevention are NonDihydropyridine calcium channel blockers?

A

Diltiazem and Verapamil (used to depress the heart at the nodal cells)

58
Q

What is the common Dihydropyridine calcium channel blocker used to treat Angina?

A

Nifedipine (mainly used to dilate vessels)

59
Q

How do beta blockers work to decrease angina?

A

They block epinephrine stimulation of myocardium, they have (-) inotropic and chronotropic effect to lower the heart rate which causes an increase in coronary perfusion. Its main use is in classic angina to depress the heart and reduce oxygen usage.

60
Q

How do Beta blockers increase myocardial perfusion?

A

They slow down the heart rate, allowing the heart to spend more time in diastole, causing an increase in perfusion. Perfusion of the myocardium can only happen during diastole. This increases preload increases oxygen demand. (Nitrates counter this by reducing venous return and preload)

61
Q

What are the cardioselective beta blockers?

A

Atenolol, Metoprolol and Acebutolol

62
Q

What are the non-selective Beta blockers?

A

Propanolol, carvedilol, Pindolol, and Labetolol

63
Q

What two drug classes cause Reflex Tachycardia?

A

CCB’s (dihydropyridines especially) and Nitrates

64
Q

What is the mechanism behind reflex tachycardia?

A

A significant drop in blood pressure stimulates the baroreceptor reflex and causes the HR to increase and the heart to work harder.

65
Q

How do Beta blockers counteract reflex tachycardia?

A

Beta blockers block sympathetic stimulation of the heart.

66
Q

True or False

DHP’s have no activity on cardiac conduction due to their mechanism of block.

A

True

67
Q

What are HCN channels and why are they significant?

A

They are a new CV drug target. They are cAMP-regulated cation channels that are also sensitive transmembrane voltage. They more hyperpolarized (-) the membrane is, the more the channel is open. These Channels regulate HR and restricted to nodal cells (SA and AV)

68
Q

What is the structure of HCN channels?

A

Tetrameric

69
Q

What family are HCN channel in and what cations/anions do they move?

A

They are in the pore loop cation channel family. They have non selective cation channel, and in the voltage range, they typically operate in, flux sodium and calcium in. Sensitive to cAMP levels.

70
Q

What drug class is Ivabradine in?

A

HCN channel inhibitor

71
Q

How does Ivabridine work to control Angina symptoms?

A

Slows HR, prolongs diastole to improve ventricular filling, reduces myocardial oxygen consumption, no hemodynamic or conduction abnormalities.

72
Q

How does ischemia cause sodium and calcium imbalances?

A

Ischemia causes reduced ATP production causing ionic homeostasis dysregulation. Sodium entry in the cell increases causing aberrant or reverse mode NCX activity, bringing calcium into the cell rather than extruding it out of the cell. Increased calcium entry interacts inappropriately with the contractile machinery and increases contractions during diastole, increasing LVEDP and wall stress. This reduces flow in the LV, which negatively impacts LV function and thereby increases sensitivity to further ischemia.

73
Q

How is angina prophylaxis achieved with Ranolazine?

A

Clinically effective by blocking late sodium currents in myocytes. Has useful antiarrhythmic effects.

74
Q

What are two side effects of Ranolazine?

A

Dizziness and QT prolongation

75
Q

What two HMG-CoA reductase inhibitors (statins) are pro-drugs that require enzymatic hydrolysis?

A

Lovastatin and Simvastatin

76
Q

What is the mechanism of action of statins?

A

Competetive HMG-CoA reductase. This causes increased LDL receptors, more LDL delivered to the liver, reducing plasma glucose.

77
Q

what is the mechanism of action of Aspirin?

A

irreversible inactivation of platelet COX-1. This blocks TXA2 synthesis, blocking anti-platelet activity, interfering with platelet aggregation. This lasts for 7-10 days (life of the platelet)

78
Q

What is the mechanism of action of P2Y12ADP receptor inhibitors?

A

Irreversible inhibition of P2Y12R reduces activation of GPiib/iiiaa complex. This lasts for days due to the fact that platelets do not synthesize new proteins.

79
Q

What is the mechanism of heparin?

A

Its sulfate groups are required for binding to antithrombin. This blocks clotting factors. Produced by mast cells and basophils endogenously.

80
Q

What clotting factors are inhibited by heparin?

A

thrombin, Xa, Vlla and lxa

81
Q

How long does it take for heparin to become active when give IV?

A

immediately

82
Q

What are the two main drugs used in stents?

A

Paclitaxel and sirolimus (Rapimycin)

83
Q

What is the MOA of Paclitaxel?

A

it stabilizes microtubule polymerization, thereby interfering with chromatid separation during mitosis.

84
Q

What is the MOA of Sirolimus?

A

Sirolimus complexes with FKBP12, and the complex binds to and inhibits the mTOR kinase, an essential regulator of translation and cell cycle progression.(In G1 to S transition)

Therapeutics Spring 2016 (6 decks)

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