Beta Blockers - Class II Antiarrythmics Flashcards

1
Q

What is the MOA for Beta Blockers?

A

Acts on both B1 receptor and closes L type calcium channels in phase 4 (which may lead to potential first degree AV blocks, evidenced by prolonged PT interval.

Funny channels responsible for the baseline depolarization of pacemaker cells - blocking cAMP and PKA. This is how they decrease the calcium.

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2
Q

Name the most often used selective BBs.

A

Metoprolol, Esmolol, Atenolol. Used in SVT, A-fib, A-flutter.

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3
Q

Name non-selective beta blockers and their uses.

A

Propranolol is used for performance anxiety, migraine prophylaxis, Essential tremor, Portal HTN, Thyrotoxicosis, and AV malformation.

Timolol inhibits the Beta receptor at the ciliary body to decrease aqueous humor formation in the relief of Glaucoma.

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4
Q

What 2 BBs also block the alpha-1 receptor?

A

Carvedilol and Labetalol.

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5
Q

Why would it be dangerous to use nonselective beta blockade in a Cocaine toxicity pt, an Asthmatic, or a Pheochromocytoma pt?

A

Short answer: Unopposed alpha vasoconstriction.

Cocaine blocks presynaptic reuptake of catecholamines, so the potent amount will be acting on alpha-1 receptors with dangerous unopposed alpha 1 vasoconstriction. Same would be true from the Pheochromocytoma tumor of chromaffin cells in the adrenal medulla releasing a monstrous amt of epinephrine.

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6
Q

What are ADRs associated with Beta blockers?

A

AV nodal block (1st degree) –> Bradycardia –> Acute Heart Failure. Impotence, difficulty ejaculating, CNS Sedation + Sleep alteration. Dyslipidemia.

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7
Q

Why do we not use BBs in Diabetic pts?

A

Beta blockers can mask the symptoms of hypoglycemia - the palpitations, sweating, tremors, shaking. You’re also exacerbating their hypoglycemia with a Beta blocker.

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8
Q

Why do we avoid using BBs in Prinzmetal Angina?

A

Interestingly…Beta receptors are found not only in the vasculature but especially in the coronary arteries.small coronary arteries are equipped almost exclusively with beta receptors, which mediate relaxation.

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9
Q

NE and Epi bind beta receptors in the liver to stimulate which two glucose related processes?

A

GNG and Glycogenolysis. Just like Glucagon.

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10
Q

What is the treatment for a pt with Beta blocker toxicity?

A

Saline, Glucagon, Atropine!

Immediately give Saline to increase volume and BP. And give Glucagon to restore glucose to the blood. And Atropine to negate the PNS affects on the heart.

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11
Q

Prolonging repolarization means prolonging the QT interval at phase 3 (K+ channel blockade).

A

Prolongs Action Potential, Increases Effective Refractory Period.

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12
Q

Amiodarone, just like Propranolol is very lipophilic. What are Amiodarone’s ADRs?

A

Pulm fibrosis, hepatotoxicity (very slow metabolism in liver), thyrotoxicity, corneal + skin deposits + photodermatitis that looks like inflamed blue skin.

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13
Q

Sotalol and Ibutalide are especially dangerous for what? Which class of antiarrhythmics shares this with them?

A

TdP, just like Class IA (Quinidine, Procainamide)

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14
Q

When is Epi given right before the administration of Amiodarone?

A

This is when a defibrillator is not giving you the cardioversion. Administer Epinephrine and then Amiodarone.

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