2- Cardiovascular II Flashcards by Joanna Brown

At therapeutic doses, CCBs act selectively on:

Peripheral arterioles

Arterioles and arteries of the heart

THEY DO NOT EFFECT VEINS

How well did you know this?

Not at all

Perfectly

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

Beta 1 receptors

How well did you know this?

Not at all

Perfectly

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

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

How well did you know this?

Not at all

Perfectly

What are the three big actions of CCBs?

Negative Inotrope

Negative Chronotrope

Decreases AV conduction

How well did you know this?

Not at all

Perfectly

What is the MOA of Verapamil?

Nondihydropyridine CCB: in blood vessels AND the heart

How well did you know this?

Not at all

Perfectly

What is the MOA of Nifedepine?

Dihydropyridine CCB: Acts primarily on arterioles and NOT the heart

How well did you know this?

Not at all

Perfectly

What are the five actions of Verapamil?

Arteriole Blockade: Decreased BP
Coronary artery dilation: improved coronary perfusion
SA Blockade: Reduced Heart Rate
AV blockade: Decreased conduction. MOST IMPORTANT ONE.
Myocardial blockade: decreased contractility

How well did you know this?

Not at all

Perfectly

What is the net effect of verapamil? Why?

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

How well did you know this?

Not at all

Perfectly

When is Verapamil used?

Angina

Essential HTN

Cardiac Dysrhythmias

How well did you know this?

Not at all

Perfectly

Which patients should never receive Verapamil?

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

How well did you know this?

Not at all

Perfectly

What is the MOA of Diltiazem?

Nondihydropyridine CCB: Same as Verapamil

CCs in the heart AND vessels

How well did you know this?

Not at all

Perfectly

What is the MOA of Nifedipine?

Dihydropyridine: Blocks CCs in VSM but NOT in the heart

How well did you know this?

Not at all

Perfectly

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

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

How well did you know this?

Not at all

Perfectly

How do the MOAs of Hydralazine and Nipride differ?

Hydralazine selectively dilates arterioles

Nipride dilates arterioles and veins

How well did you know this?

Not at all

Perfectly

What is the underlying cause of orthostatic hypotension?

VENOdilation

How well did you know this?

Not at all

Perfectly

Does hydralazine cause postural hypotension?

Not so much, because it ONLY EFFECTS ARTERIES

How well did you know this?

Not at all

Perfectly

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

A Thiazide Diuretic

How well did you know this?

Not at all

Perfectly

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

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

How well did you know this?

Not at all

Perfectly

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

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

How well did you know this?

Not at all

Perfectly

Aldosterone Antagonists have one major AE:

Hyperkalemia

How well did you know this?

Not at all

Perfectly

Benefits of Digoxin include:

symptomatic relief

NOT A FIRST LINE AGENT

How well did you know this?

Not at all

Perfectly

What is the MOA for digoxin?

Inhibits Na-K ATPase, promoting calcium accumulation within myocytes

the calcium augments contractile force

How well did you know this?

Not at all

Perfectly

What is the relationship between potassium levels and digoxin effect?

Potassium competes with dig for binding

It potassium levels are low, dig is hyperactive

If potassium levels are high, dig is hypoactive

How well did you know this?

Not at all

Perfectly

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

Antidysrhythmics - have cardiosuppressant and prodysrhythmic actions that can worsen HF

CCBs: Can make HF worse EXCEPT Norvasc

NSAIDs: promote sodium retention and peripheral vasoconstriction

How well did you know this?

Not at all

Perfectly

The cardiac effects of Beta blockers are nearly identical to:

the effects of CCBs

Class I Antidysrhythmics are:

Sodium Channel Blockers Slow impulse conduction in the SA, AV, and Purkinjes

Class II Antidysrhythmics are:

Beta Blockers

Class III antidysrhythmics are:

Potassium Channel Blockers

Class IV Antidysrhythmics are:

CCBs

**Class 1B** Prototype MOA

Lidocaine Accelerates Repolarization

Amiodarone carries a black box warning for:

Pulmonary Toxicity AND Liver Toxicity

**CLASS III** Prototype MOA

Potassium Channel Blockers Amiodarone Delays repolarization of rapid action potentials

How will potassium channel blockers alter the ECG?

They prolong repolarization, so they'll prolong the QT

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

Verapamil Diltiazem

Blockade of calcium channels in the heart has three effects:

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

CCBs are not indicated for:

ventricular dysrhythmias They only effect the SA and AV conduction

Moderate cardiac atherosclerotic disease usually first manifests as:

Angina

What is the function of lipoproteins in the body\>

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

What is the role of LDLs in the body?

delivering cholesterol to non-hepatic tissues

Which lipoprotein makes the greatest contribution to coronary artery disease?

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

What is the function of HDLs in the body?

Take cholesterol from the peripheral tissues and return it to the liver *Promote cholesterol Removal!*

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

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

What happens when macrophages ingest oxidized LDLs?

They become *foam cells*: contain large vacuoles filled with cholesterol They accumulate beneath the arterial epithelium and form a *fatty streak*

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

An immature one Once the fibrous cap is well established, it's unusual for a thrombus to develop

Atherosclerosis involves cholesterol, but it is primarily a ________ disease

chronic inflammatory

Is diabetes a risk factor for developing atherosclerotic disease?

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

What are the four behavior modifications proven to reduce LDLs?

Diet Exercise Weight Control Smoking Cessation

Metabolic Syndrome Includes:

Three or more of the following: 1. High TG levels 2. Low HDL levels 3. Hyperglycemia 4. Hypertension 5. Waist circumference

What is the other name for Statins?

HMG-CoA Reductase Inhibitors

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

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

What is the MOA of statins?

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

What are the therapeutic uses of statins?

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!)

Statins are primarily excreted by:

the liver, into the bile

What are the major adverse effects of Statins?

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

What should be done if a statin is causing myalgia?

Replacing Vitamin D Switching Statins Coenzyme Q10

Which patients with impaired liver function can take statins?

Patients with viral or alcoholic hepatitis CANNOT Patients with NASH CAN and SHOULD (they actually help halt the disease process)

Which statins are preferred with renal disease?

Atorvastatin and Fluvastatin

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

Will probably need a lower dose, especially with Rosuvastatin Start with the lowest available dosage and monitor closely

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

Bile acid sequestrants

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

Hepatitis and Pregnancy

What is the prototypical bile acid sequestrant?

Ezetimibe

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

monoclonal antibody