Pharmacology Flashcards

1
Q

Anti-adrenergic will interfere with the SNS where?

A

Central nervous system
Postganglionic sympathetic nerve ending
Peripheral alpha- & beta-receptors

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2
Q

When SNS is stimulated, it will release norepinephrine that will stimulates what?

A

Post-synaptic alpha- & beta- adrenergic receptors

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3
Q

Cardiac output and peripheral vascular resistance are controlled by which system?

A

Sympathetic Nervous System

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4
Q

Activation of alpha-1 receptor leads to what?

A

Vasoconstriction

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5
Q

Where are the alpha-1 receptors?

A

Vascular smooth muscles

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6
Q

Activation of alpha-2 receptor leads to what?

A

Vasoconstriction

Decrease in norepinephrine release

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7
Q

Where are the alpha-2 receptors?

A

Presynaptic adrenergic nerve terminal

Vascular smooth muscle

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8
Q

Activation of beta-1 receptor leads to what?

A
Increase heart rate
Increase contractility
Increase renin release
Stimulate lipolysis
Speeds up the atrioventricular node conduction
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9
Q

Where are the beta-1 receptors?

A

Heart
Presynaptic adrenergic nerve terminal
Kidneys

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10
Q

Activation of beta-2 receptor leads to what?

A

Vasodilatation
Bronchodilatation
Stimulate glygogenolysis

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11
Q

Where are the beta-2 receptors?

A

Vascular smooth muscle
Liver
Bronchial smooth muscle

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12
Q

Central adrenergic inhibitors (CNS alpha-2 agonists) will do what?

A

Diminish peripheral vascular resistance
Decrease cardiac output
Decrease heart rate and blood pressure

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13
Q

What kind of drug should you give to a patient if you want to inhibit the uptake of norepinephrine or reduce the force of myocardial contraction?

A

Sympathetic nerve ending antagonist

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14
Q

What are the main side-effect of sympathetic nerve ending antagonist?

A

Sedation
Impaired concentration
Psychotic depression

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15
Q

Non-selective blockage of alpha-1 receptor with a peripheral alpha-adrenergic receptor antagonist will lead to what?

A
Vasodilatation
Increase in heart rate mediated by baroreceptors
Undesired reflex tachycardia
Postural hypotension
Headaches/dizziness
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16
Q

Non-selective blockage of alpha-2 receptor with a peripheral alpha-adrenergic receptor antagonist will lead to what?

A

Reduction in norepinephrine
Undesired reflex tachycardia
Postural hypotension
Headaches/dizziness

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17
Q

Selective blockage of alpha-1 receptor with a peripheral alpha-adrenergic receptor antagonist will lead to what? What is it good for?

A

Vasodilatation
Postural hypotension
Headaches/dizziness
good for: hypertension

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18
Q

What is the third-line of treatment for heart disease?

A

Beta-adrenergic receptor antagonists

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19
Q

What are the major effects of beta-blockage?

A

Lowers inotropy
Lowers heart rate
Lowers conduction velocity

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20
Q

Non-selective beta-adrenergic receptor antagonists will lead to bronchospasm and bronchovaconstriction. Which beta-selective drug does not do that?

A

Beta-1 selective

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21
Q

What is the clinical use of beta-adrenergic receptor antagonists?

A

Ischemic heart disease
Hypertension
Heart failure
Tachyarrhythmia

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22
Q

What should you use for hypertension?

A

Alpha-blockers

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23
Q

Name two beta-blockers drugs that also have alpha-blockers properties

A

Labetolol

Carvedilol

24
Q

According to the Vaughan Williams classification, what are class 1 drugs and what do they do?

A

Sodium channel blockers
Reduce automaticity and/or conduction velocity in fast channel tissue (ventricular and atrial muscles, His-Purkinje system)

25
Q

According to the Vaughan Williams classification, what are class 2 drugs and what do they do?

A

Beta-adrenergic receptors blockers

Acts on slow channel tissues (sinus and atrioventricular nodes)

26
Q

According to the Vaughan Williams classification, what are class 3 drugs and what do they do?

A

Potassium channel blockers

Increase action potential duration in fast channel tissue (ventricular and atrial muscles, His-Purkinje system)

27
Q

According to the Vaughan Williams classification, what are class 4 drugs and what do they do?

A

Calcium channel blockers

Acts on slow-channel tissues (sinus and atrioventricular nodes)

28
Q

On the ECG, what is the conduction time through the AV node?

A

The PR interval

29
Q

On the ECG, slower ventricular conduction will show what?

A

A longer QRS complex

30
Q

What is Vagal enhancement and what does it do?

A

Enhancement of basal K+ current

Hyperpolarize the cell to take it away from firing threshold

31
Q

With respect to calcium, what does a beta-blocker do?

A

Remove Ca2+ current

32
Q

What do purinergic agonists do?

A

Produce “Vagal-like effect” via purinergic receptor activation

33
Q

What are the effects of class 2 & 4 drugs on the ECG?

A

PR interval in made longer

Heart rate is diminished

34
Q

Are drugs of class 2 & 4 recommended for atrial fibrillation?

A

Yes. Atrial fibrillation is determined by the atrioventricular node refractory period. Increasing this refractory period will reduce ventricular response and symptoms

35
Q

Are beta-blockers drugs useful for atrioventricular node reentry termination and/or atrial fibrillation termination?

A

No that much for reentry
Absolutely not for atrial fibrillation termination
Good for prevention

36
Q

Is vagal enhancement useful for atrial fibrillation?

A

No

37
Q

Is vagal enhancement useful for atrioventricular node reentry termination?

A

Yes

38
Q

Is vagal enhancement useful for rate control?

A

Yes

39
Q

Is Ca2+ channel blockers useful for atrial fibrillation?

A

No

40
Q

Is Ca2+ channel blockers useful for atrioventricular node reentry termination?

A

Really useful

41
Q

Is Ca2+ channel blockers useful to slow ventricular response rate?

A

Yes

42
Q

In terms of treatment, what is the disadvantage of purinergic agonists?

A

They are very temporary

43
Q

Are purinergic agonists useful for atrioventricular node reentry termination?

A

Highly effective (but not for prevention)

44
Q

Are purinergic agonists useful for atrial fibrillation termination?

A

No

45
Q

Are purinergic agonists useful for ventricular rate control?

A

No

46
Q

Beta-blockers, Vagal enhancement, Ca2+ channel blockers, Purinergic agonists belong to which class of drugs?

A

Class 2 and 4

47
Q

What are the effects of class 3 drugs on the ECG?

A

Increase of the QT interval

48
Q

What are the effects of class 1 drugs on the ECG?

A

Increase of the QRS complex duration

49
Q

How does a class 3 drug terminate reentry?

A

By increasing refractory period

50
Q

What is the most important determinant of refractory period in fast channel tissues?

A

Action potential duration

51
Q

How does a class 1 drug decreases DAD arrythmia?

A

Supresses extrasystoles (premature ventricular and atrial contractions) that can act as triggers

52
Q

What are the most effective drugs for atrial fibrillation on the long term?

A
Amiodarone (class 1 to 4)
Sotalol (class 2 & 3, but increases risk of long QT syndrome)
53
Q

What is the most effective drug for ventricular tachycardia on the long term?

A

Amiodarone (class 1 to 4)

54
Q

CPVT is a congenital ventricular tachycardia syndrome, and is caused by what? What drug is useful to treat it?

A

Ryanodine receptor mutation

Beta-blocker is useful

55
Q

Long QT syndrome is a congenital ventricular tachycardia syndrome. What drug is useful to treat it?

A

Beta-blocker is useful. If not, go for the implanted defibrillator

56
Q

Acquired ventricular tachycardia requires what to correct it?

A

Intravenous lidocaine/amiodarone

Direct current