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
According to the Vaughan Williams classification, what are class 2 drugs and what do they do?
Beta-adrenergic receptors blockers | Acts on slow channel tissues (sinus and atrioventricular nodes)
26
According to the Vaughan Williams classification, what are class 3 drugs and what do they do?
Potassium channel blockers | Increase action potential duration in fast channel tissue (ventricular and atrial muscles, His-Purkinje system)
27
According to the Vaughan Williams classification, what are class 4 drugs and what do they do?
Calcium channel blockers | Acts on slow-channel tissues (sinus and atrioventricular nodes)
28
On the ECG, what is the conduction time through the AV node?
The PR interval
29
On the ECG, slower ventricular conduction will show what?
A longer QRS complex
30
What is Vagal enhancement and what does it do?
Enhancement of basal K+ current | Hyperpolarize the cell to take it away from firing threshold
31
With respect to calcium, what does a beta-blocker do?
Remove Ca2+ current
32
What do purinergic agonists do?
Produce "Vagal-like effect" via purinergic receptor activation
33
What are the effects of class 2 & 4 drugs on the ECG?
PR interval in made longer | Heart rate is diminished
34
Are drugs of class 2 & 4 recommended for atrial fibrillation?
Yes. Atrial fibrillation is determined by the atrioventricular node refractory period. Increasing this refractory period will reduce ventricular response and symptoms
35
Are beta-blockers drugs useful for atrioventricular node reentry termination and/or atrial fibrillation termination?
No that much for reentry Absolutely not for atrial fibrillation termination Good for prevention
36
Is vagal enhancement useful for atrial fibrillation?
No
37
Is vagal enhancement useful for atrioventricular node reentry termination?
Yes
38
Is vagal enhancement useful for rate control?
Yes
39
Is Ca2+ channel blockers useful for atrial fibrillation?
No
40
Is Ca2+ channel blockers useful for atrioventricular node reentry termination?
Really useful
41
Is Ca2+ channel blockers useful to slow ventricular response rate?
Yes
42
In terms of treatment, what is the disadvantage of purinergic agonists?
They are very temporary
43
Are purinergic agonists useful for atrioventricular node reentry termination?
Highly effective (but not for prevention)
44
Are purinergic agonists useful for atrial fibrillation termination?
No
45
Are purinergic agonists useful for ventricular rate control?
No
46
Beta-blockers, Vagal enhancement, Ca2+ channel blockers, Purinergic agonists belong to which class of drugs?
Class 2 and 4
47
What are the effects of class 3 drugs on the ECG?
Increase of the QT interval
48
What are the effects of class 1 drugs on the ECG?
Increase of the QRS complex duration
49
How does a class 3 drug terminate reentry?
By increasing refractory period
50
What is the most important determinant of refractory period in fast channel tissues?
Action potential duration
51
How does a class 1 drug decreases DAD arrythmia?
Supresses extrasystoles (premature ventricular and atrial contractions) that can act as triggers
52
What are the most effective drugs for atrial fibrillation on the long term?
``` Amiodarone (class 1 to 4) Sotalol (class 2 & 3, but increases risk of long QT syndrome) ```
53
What is the most effective drug for ventricular tachycardia on the long term?
Amiodarone (class 1 to 4)
54
CPVT is a congenital ventricular tachycardia syndrome, and is caused by what? What drug is useful to treat it?
Ryanodine receptor mutation | Beta-blocker is useful
55
Long QT syndrome is a congenital ventricular tachycardia syndrome. What drug is useful to treat it?
Beta-blocker is useful. If not, go for the implanted defibrillator
56
Acquired ventricular tachycardia requires what to correct it?
Intravenous lidocaine/amiodarone | Direct current