Pharmacology Flashcards

1
Q

What are the ANS action on the CV system?

A

Sympathetic:

  • Peripheral resistance
  • HR
  • Force (contractility)
  • Venous tone

Parasympathetic:

  • HR
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

The modulation of adrenergic receptors can be done is 4 sites. What are those and explain the mechanism.

A
  1. Sympathetic nerve-ending antagonist
    Inhibits uptake of NE into storage vesicles in post-ganglionic and central neurons leading to NE degradation: ↓ myocardial contraction and TPR but MANY side effects, no longer used
  2. CNS α 2 agonist
    We don’t use anymore because of side effects
  3. ß-Receptor blockers
    Act on the heart, used for more chronic conditions, ß-1 is better because no activity on lungs (ß2)
    Partial ß-agonist do not slow the heart as much
    Clinical uses: ischemic heart disease, hypertension, heart failure, tachyarrhythmia
  4. Peripheral α receptors
  • Non-selective: too much side effects (undesired tachycardia)
  • Selective: better choice
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

α 1 receptors: give the type of distribution, the response and the drugs that act on it.

A

Type of distribution: Vascular smooth muscle (arterioles and veins) PERIPHERY

Response: Vasoconstriction because of calcium activation

Drugs:

Prazosin

Terazosin

Doxazosin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

α 2 receptors: give the type of distribution, the response and the drugs that act on it.

A

Type of distribution: Presynaptic adrenergic nerve terminals, vascular smooth muscles (coronary and renal arterioles) CENTRAL

Response: Inhibition of NE release, Decreases Camp so does the opposite of B receptors

Drugs: Clonidine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

ß 1 receptors: give the type of distribution, the response and the drugs that act on it.

A

Type of distribution: Heart, kidney, presynaptic adrenergic nerve terminal, adipose tissue

Response:

↑ HR

↑ Contractility

↑ AV node conduction

↑ NE release

↑ Lipolysis

Drugs:

Non-elective: Propanolol, Caarvedilol, Labetalol

Selective: Matoprolol, Bisoprolol, Atenolol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

ß 2: give the type of distribution, the response and the drugs that act on it.

A

Type of distribution: Vascular smooth muscle (arterioles except skin and liver), bronchial smooth muscle, liver

Response:

Vasodilation

Bronchodilation

Glycogenolysis

Drugs:

? pas donné d’exemple en classe

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the clinical use of Beta Blockers?

A
  • —Ischemic heart disease

—Decrease myocardial oxygen demand by reducing heart rate, blood pressure (afterload) and contractility. It improves survival following acute myocardial infarction

  • —Hypertension
    —Not usually used as first line therapy for HTN unless another indication for their use exists (e.g. coronary artery disease)
  • —Heart Failure
    —Metoprolol, bisoprolol, and carvedilol have been shown to decrease mortality in patients with heart failure with reduced ejection fraction
  • —Tachyarrhythmia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Describe classe 1 of Vaughan Williams Classification of Antiarrhythmic Drug Action

A

Class I:

Na2+ channel blockers- reduce automaticity and/or conduction velocity in fast channel tissue; FAST CHANNEL

EX: propafenone, flecainide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Describe classe 2 of Vaughan Williams Classification of Antiarrhythmic Drug Action

A

Class II:

ß-blockers - SLOW CHANNEL

EX: propranolol, metoprolol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Describe classe 3 of Vaughan Williams Classification of Antiarrhythmic Drug Action

A

Class III:

K+ channel blockers- increase APD in fast channel tissue FAST CHANNEL

EX: sotalol, amiodarone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Describe classe 4 of Vaughan Williams Classification of Antiarrhythmic Drug Action

A

Class IV:

Ca+ channel blockers - act predominantly on SLOW CHANNEL

EX: verapamil, diltiazem

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

True or false: some drugs are part of more than 1 class.

A

True. Many drugs have actions of more than one class: sotalol has class 2 and class 3 actions; amiodarone has class 1, 2, 3 and 4 actions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the effect of class 2 and 4 on HR, PR, QRS and QT ?

A

Heart Rate:

PR (AV node conduction):

QRS (Ventricular conduction): /

QT (Ventricular activation to repolarization): /

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the 4 Mmechanism by which drugs depress slow channel tissue action potentials ?

A
  1. Βeta-blockers
  2. Vagal enhancers
  3. Ca2+ channel blockers (verapamil, diltiazem)
  4. Purinergic agonists (adenosine)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the effect of Βeta-blockers on AVN reentry termination, prevention, AF termination and AF rate control ?

A

Mechanism: Removes Ca2+

AVN reentry termination: ±

AVN reentry prevention: ±

AF termination: -

AF rate control: ++

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the effect of Vagal enhancers on AVN reentry termination, prevention, AF termination and AF rate control ?

A

Mechanism: Enhances a basal K+ current

AVN reentry termination: +

AVN reentry prevention: ±

AF termination: -

AF rate control: ++

17
Q

What is the effect of Ca2+ channel blockers on AVN reentry termination, prevention, AF termination and AF rate control ?

A

Mechanism: Reduce Ca2+ entry

AVN reentry termination: +++

AVN reentry prevention: +

AF termination: -

AF rate control: ++

DRUGS: verapamil and diltiazem

18
Q

What is the effect of a Purinergic agonists on AVN reentry termination, prevention, AF termination and AF rate control ?

A

Mechanism: Vagal-like effects

AVN reentry termination: +++

AVN reentry prevention: -

AF termination: -

AF rate control: -

DRUGS: adenosine

19
Q

What is the effect of class 1 and 3 drugs on HR, PR, QRS and QT ?

A

Heart Rate: /

PR (AV node conduction): /

QRS (Ventricular conduction): ↑

QT (Ventricular activation to repolarization): ↑

20
Q

What isthe most important determinant of refractory period in fast channel tissue?

A

The action potential duration (APD).

21
Q

What is the most effective drug for ventricular tachycardia and atrial fibrillation but is a drug of last resort because of side effects?

A

Amiodarone

22
Q

What are the 2 ways to prevent or terminate sustained tachyarrhythmias such as atrial fibrilation?

A
  1. Decreased automatic or DAD arrhythmia (class I agents) by suppressing triggers of re-entry and decrease enhanced automaticity
  2. Increased refractory period (class III agents) by terminate re-entry