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Pharmacology I > 2- Cardiovascular II > Flashcards

2- Cardiovascular II Flashcards

1
Q

At therapeutic doses, CCBs act selectively on:

A

Peripheral arterioles

Arterioles and arteries of the heart

THEY DO NOT EFFECT VEINS

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2
Q

Calcium channels in the myocardium, SA node, and AV node are activated by:

A

Beta 1 receptors

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3
Q

How do the actions of CCBs and Beta Blockers on the heart differ?

A

They don’t! They’re targeting the exact same thing

CCBs are stopping calcium channels from responding to Beta 1 activation

Beta blockers are preventing that activation from taking place to begin with

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4
Q

What are the three big actions of CCBs?

A

Negative Inotrope

Negative Chronotrope

Decreases AV conduction

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5
Q

What is the MOA of Verapamil?

A

Nondihydropyridine CCB: in blood vessels AND the heart

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6
Q

What is the MOA of Nifedepine?

A

Dihydropyridine CCB: Acts primarily on arterioles and NOT the heart

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7
Q

What are the five actions of Verapamil?

A
  1. Arteriole Blockade: Decreased BP
  2. Coronary artery dilation: improved coronary perfusion
  3. SA Blockade: Reduced Heart Rate
  4. AV blockade: Decreased conduction. MOST IMPORTANT ONE.
  5. Myocardial blockade: decreased contractility
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8
Q

What is the net effect of verapamil? Why?

A

Verapamil triggers baroreceptor reflexes, which tends to neutralize the HR, Conduction, and contractility effects

The only thing that dramatically changes, then, is vasodilation and increased coronary perfusion

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9
Q

When is Verapamil used?

A

Angina

Essential HTN

Cardiac Dysrhythmias

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10
Q

Which patients should never receive Verapamil?

A

Patients with sick sinus syndrome or 2nd or 3rd degree block

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11
Q

What is the MOA of Diltiazem?

A

Nondihydropyridine CCB: Same as Verapamil

CCs in the heart AND vessels

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12
Q

What is the MOA of Nifedipine?

A

Dihydropyridine: Blocks CCs in VSM but NOT in the heart

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13
Q

Which drug will most likely increase a patient’s heart rate: Diltiazem or Nifedipine?

A

Nifedipine

Both of them trigger reflex tachycardia from vasodilation, but only Diltiazem has cardio-suppressive effects. In the case of Nifedipine, that reflex tachycardia is unopposed

If you give Nifedipine as a slow release, really isn’t a problem

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14
Q

How do the MOAs of Hydralazine and Nipride differ?

A

Hydralazine selectively dilates arterioles

Nipride dilates arterioles and veins

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15
Q

What is the underlying cause of orthostatic hypotension?

A

VENOdilation

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16
Q

Does hydralazine cause postural hypotension?

A

Not so much, because it ONLY EFFECTS ARTERIES

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17
Q

If a patient presents with essential hypertension and no compelling indications, what is the first line drug?

A

A Thiazide Diuretic

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18
Q

Why would you want to combine a vasodilator with a beta blocker?

A

You can negate the reflex tachycardia caused by the vasodilator with the beta blocker

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19
Q

In addition to salt and water retention, why is RAAS activation so deleterious in heart failure?

A

It promotes remodeling and fibrosis, impairing pumping and increasing the probability of dysrhythmias

Activates the SNS and inhibits NE uptake in the heart

promotes vascular fibrosis

Promotes baroreceptor dysfunction

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20
Q

Aldosterone Antagonists have one major AE:

A

Hyperkalemia

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21
Q

Benefits of Digoxin include:

A

symptomatic relief

NOT A FIRST LINE AGENT

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22
Q

What is the MOA for digoxin?

A

Inhibits Na-K ATPase, promoting calcium accumulation within myocytes

the calcium augments contractile force

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23
Q

What is the relationship between potassium levels and digoxin effect?

A

Potassium competes with dig for binding

It potassium levels are low, dig is hyperactive

If potassium levels are high, dig is hypoactive

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24
Q

Patients with HF signs and symptoms should not take which three drugs? Why?

A

Antidysrhythmics - have cardiosuppressant and prodysrhythmic actions that can worsen HF

CCBs: Can make HF worse EXCEPT Norvasc

NSAIDs: promote sodium retention and peripheral vasoconstriction

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25
Q

The cardiac effects of Beta blockers are nearly identical to:

A

the effects of CCBs

26
Q

Class I Antidysrhythmics are:

A

Sodium Channel Blockers

Slow impulse conduction in the SA, AV, and Purkinjes

27
Q

Class II Antidysrhythmics are:

A

Beta Blockers

28
Q

Class III antidysrhythmics are:

A

Potassium Channel Blockers

29
Q

Class IV Antidysrhythmics are:

A

CCBs

30
Q

Class 1B

Prototype

MOA

A

Lidocaine

Accelerates Repolarization

31
Q

Amiodarone carries a black box warning for:

A

Pulmonary Toxicity

AND

Liver Toxicity

32
Q

CLASS III

Prototype

MOA

A

Potassium Channel Blockers

Amiodarone

Delays repolarization of rapid action potentials

33
Q

How will potassium channel blockers alter the ECG?

A

They prolong repolarization, so they’ll prolong the QT

34
Q

Only to calcium channel blockers are able to block Ca channels in the heart:

A

Verapamil

Diltiazem

35
Q

Blockade of calcium channels in the heart has three effects:

A
  1. Slowing of SA node automaticity
  2. Delay of AV conduction
  3. Reduced contractility
36
Q

CCBs are not indicated for:

A

ventricular dysrhythmias

They only effect the SA and AV conduction

37
Q

Moderate cardiac atherosclerotic disease usually first manifests as:

A

Angina

38
Q

What is the function of lipoproteins in the body>

A

Binding to fats (which are insoluble) and transporting them in the blood

39
Q

What is the role of LDLs in the body?

A

delivering cholesterol to non-hepatic tissues

40
Q

Which lipoprotein makes the greatest contribution to coronary artery disease?

A

LDLs

For every 1% drop in LDL levels, the risk for ACS reduces 1%

41
Q

What is the function of HDLs in the body?

A

Take cholesterol from the peripheral tissues and return it to the liver

Promote cholesterol Removal!

42
Q

Why is it so problematic to have high levels of LDLs?

A

The real problems arise when LDLs enter the subendothelium and become oxidized

Once oxidized, they:

  1. Attract monocytes, which morph into macrophages
  2. Inhibit macrophage mobility, thereby trapping them at the site of atherogenesis
  3. Undergo uptake by macrophages (which only eat oxidized LDLs)
  4. Damage the vascular endothelium, as they are cytotoxic
43
Q

What happens when macrophages ingest oxidized LDLs?

A

They become foam cells: contain large vacuoles filled with cholesterol

They accumulate beneath the arterial epithelium and form a fatty streak

44
Q

Which is more likely: having an infarction develop at the site of a mature lesion or an immature one?

A

An immature one

Once the fibrous cap is well established, it’s unusual for a thrombus to develop

45
Q

Atherosclerosis involves cholesterol, but it is primarily a ________ disease

A

chronic inflammatory

46
Q

Is diabetes a risk factor for developing atherosclerotic disease?

A

No, it is considered a risk equivalent

If you have diabetes, it doesn’t matter if you have or do not have risk factors. You are automatically considered at risk for having a heart attack due to atherosclerotic disease

47
Q

What are the four behavior modifications proven to reduce LDLs?

A

Diet

Exercise

Weight Control

Smoking Cessation

48
Q

Metabolic Syndrome Includes:

A

Three or more of the following:

  1. High TG levels
  2. Low HDL levels
  3. Hyperglycemia
  4. Hypertension
  5. Waist circumference
49
Q

What is the other name for Statins?

A

HMG-CoA Reductase Inhibitors

50
Q

Aside from balancing cholesterol and TG levels, what are the positive benefits of Statins?

A
  1. Reduce inflammation at plaque sites
  2. Stabilize existing plaque sites
  3. Inhibit platelet deposition and aggregation
  4. Suppress production of thrombin
51
Q

What is the MOA of statins?

A
  1. Inhibit synthesis of new LDLs by inhibiting HMG-CoA Reductase (the rate limiting enzyme in LDL production)
  2. Increase the number of LDL receptors on hepatocytes, making the liver more capable of breaking down cholesterol
52
Q

What are the therapeutic uses of statins?

A
  1. Hypercholesterolemia (obviously)
  2. Prevention of CV events (both in people who have and have not yet had an event)
  3. Primary prevention in people with normal LDL levels but increased risk
  4. Post-MI
  5. Diabetes (controlling CV risk factors is just as important as controlling high BG!)
53
Q

Statins are primarily excreted by:

A

the liver, into the bile

54
Q

What are the major adverse effects of Statins?

A
  1. Myopathy and Rhabdomyolysis
  2. Hepatotoxicity
  3. New-onset diabetes
55
Q

What should be done if a statin is causing myalgia?

A

Replacing Vitamin D

Switching Statins

Coenzyme Q10

56
Q

Which patients with impaired liver function can take statins?

A

Patients with viral or alcoholic hepatitis CANNOT

Patients with NASH CAN and SHOULD (they actually help halt the disease process)

57
Q

Which statins are preferred with renal disease?

A

Atorvastatin and Fluvastatin

58
Q

If you need to start a statin in an Asian patient, what should you keep in mind?

A

Will probably need a lower dose, especially with Rosuvastatin

Start with the lowest available dosage and monitor closely

59
Q

Which drugs are used as adjuncts to statins when therapy is insufficient with a statin alone?

A

Bile acid sequestrants

60
Q

For which patient populations do the risk of statins far outweigh the benefits

A

Hepatitis and Pregnancy

61
Q

What is the prototypical bile acid sequestrant?

A

Ezetimibe

62
Q

If you see a drug that ends in -cumab, you should think:

A

monoclonal antibody

Pharmacology I (29 decks)

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