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?

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