Heart drugs Flashcards

1
Q

How do Beta-blockers decrease HR?

A

Decrease If and Ica

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2
Q

How do Calcium-channel blockers decrease HR?

A

Decrease Ica

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3
Q

How does Ivabradine decrease HR?

A

Decrease If

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4
Q

Do beta-blockers decrease contractility? If so, how?

A

Yes- decrease cAMP. This decreases Ca sensitaization of Troponin C by PKA, decreases DHPR Ca channel open and decreases Ca ATPase (on SR) activity

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5
Q

Do calcium- channel blockers decreases contractility?

A

Yes- all types do

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6
Q

Does ivabradine decrease contractility? If so, how?

A

No- on decreases If so only affects SAN conduction, so only affects HR not contractility

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7
Q

Whats the difference between phenylakylamines and benzothiazepines, and dihydropyridines?

A

Phenylakylamines and benzothiazipines are rate slowing (alos affect contractility) CCBs and dihydropyridines are non-rate slowing CCBs (just affect SM contractility)

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8
Q

What is veramapil and what does it do?

A

A phenylakylamine CCB- decreases HR

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9
Q

What is dialtiazem and what does it do?

A

A benzothiazepine CCB- decreases HR

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10
Q

What is amlodipine and what does it do?

A

A dyhyrdropyridine CCB- decreases contractility of vascular SM

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11
Q

What effect can dihydropryridines have on HR?

A

They cause potent vasodilation which can cause reflex tachycardia via decreased firing of baroreceptors.

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12
Q

What would you use a organic nitrate for and how does it work?

A

To dilate the coronary vessels (increase myocardial oxygen supply) by increasing cGMP via guanyl cyclase activation

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13
Q

What would you use a potassium channel opener for and why does it work?

A

To dilate the coronary vessels (increase myocardial oxygen supply) by increasing potassium efflux, polarization of the SM cell, impairs ability to contract.

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14
Q

Give two side effects of verapamil?

A

Brdycardia, constipation

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15
Q

Give 3 side effects of dihydropyridines?

A

Ankle odema, headache/flushing and palpitations (reflex tachycardia)

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16
Q

What is the RMP of ventricular mycoyte?

A

-65mV

17
Q

In the Vaughan Williams classification, what is class 1?

A

Sodium channel blockers (usually open to cause fast depolarisation)

18
Q

In the Vaughan Williams classification, what is class 2?

A

Beta blockers

19
Q

In the Vaughan Williams classification, what is class 3?

A

Membrane stabilisation/ blaockade of K channels (which cause slow repolorisation)

20
Q

In the Vaughan Williams classification, what is class 4?

A

CCBs- they usually cause maintain depolarisation as well as enhance contractility.

21
Q

Name 4 anti-arrythmic drugs

A

Adenosine, verapamil, amiodarone and digoxin

22
Q

What is adenosine used to treat and how does it work?

A

Arrythmia- Binds to Gs on VSM, causing relaxation and binds to Gi on SAN, decreasing HR.

23
Q

What is verapamil used to treat and how does it work?

A

Arrythmia- its a phenylakylamine CCB (so rate slowing). Used specifically to decrease ventricualr responsiveness to atrial arrythmias. Verapamil protects your Ventricular rate.

24
Q

What is amiodarone used to treat and how does it work? Name 3 side effects

A

Arrythmia- spraventricualr and ventriular tachycardias because it prevents re-entry. manily by K channel bloackade, which prolongs repolarisation. Photosensitove skin rashes, thyroid conditions and pulmonary fibrosis.

25
Q

What is digoxin used for and how does it work? Name an important consideration.

A

Arrythmia, specifically atrial fibrillation or flutter (–> decreased CO) - cardiac glycoside, central vagal stimulation increases refractory period and decrease conduction through AVN. It also inhibits the Na/K ATPase, which enhances intracllualr Ca concentration- hypokalemia increases its toxicoty