Pharmacology Flashcards
What are the ANS action on the CV system?
Sympathetic:
- Peripheral resistance
- HR
- Force (contractility)
- Venous tone
Parasympathetic:
- HR
The modulation of adrenergic receptors can be done is 4 sites. What are those and explain the mechanism.
-
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 -
CNS α 2 agonist
We don’t use anymore because of side effects -
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 - Peripheral α receptors
- Non-selective: too much side effects (undesired tachycardia)
- Selective: better choice
α 1 receptors: give the type of distribution, the response and the drugs that act on it.
Type of distribution: Vascular smooth muscle (arterioles and veins) PERIPHERY
Response: Vasoconstriction because of calcium activation
Drugs:
Prazosin
Terazosin
Doxazosin
α 2 receptors: give the type of distribution, the response and the drugs that act on it.
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
ß 1 receptors: give the type of distribution, the response and the drugs that act on it.
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
ß 2: give the type of distribution, the response and the drugs that act on it.
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
What are the clinical use of Beta Blockers?
- 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
Describe classe 1 of Vaughan Williams Classification of Antiarrhythmic Drug Action
Class I:
Na2+ channel blockers- reduce automaticity and/or conduction velocity in fast channel tissue; FAST CHANNEL
EX: propafenone, flecainide
Describe classe 2 of Vaughan Williams Classification of Antiarrhythmic Drug Action
Class II:
ß-blockers - SLOW CHANNEL
EX: propranolol, metoprolol
Describe classe 3 of Vaughan Williams Classification of Antiarrhythmic Drug Action
Class III:
K+ channel blockers- increase APD in fast channel tissue FAST CHANNEL
EX: sotalol, amiodarone
Describe classe 4 of Vaughan Williams Classification of Antiarrhythmic Drug Action
Class IV:
Ca+ channel blockers - act predominantly on SLOW CHANNEL
EX: verapamil, diltiazem
True or false: some drugs are part of more than 1 class.
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
What is the effect of class 2 and 4 on HR, PR, QRS and QT ?
Heart Rate: ↓
PR (AV node conduction): ↑
QRS (Ventricular conduction): /
QT (Ventricular activation to repolarization): /
What are the 4 Mmechanism by which drugs depress slow channel tissue action potentials ?
- Βeta-blockers
- Vagal enhancers
- Ca2+ channel blockers (verapamil, diltiazem)
- Purinergic agonists (adenosine)
What is the effect of Βeta-blockers on AVN reentry termination, prevention, AF termination and AF rate control ?
Mechanism: Removes Ca2+
AVN reentry termination: ±
AVN reentry prevention: ±
AF termination: -
AF rate control: ++
What is the effect of Vagal enhancers on AVN reentry termination, prevention, AF termination and AF rate control ?
Mechanism: Enhances a basal K+ current
AVN reentry termination: +
AVN reentry prevention: ±
AF termination: -
AF rate control: ++
What is the effect of Ca2+ channel blockers on AVN reentry termination, prevention, AF termination and AF rate control ?
Mechanism: Reduce Ca2+ entry
AVN reentry termination: +++
AVN reentry prevention: +
AF termination: -
AF rate control: ++
DRUGS: verapamil and diltiazem
What is the effect of a Purinergic agonists on AVN reentry termination, prevention, AF termination and AF rate control ?
Mechanism: Vagal-like effects
AVN reentry termination: +++
AVN reentry prevention: -
AF termination: -
AF rate control: -
DRUGS: adenosine
What is the effect of class 1 and 3 drugs on HR, PR, QRS and QT ?
Heart Rate: /
PR (AV node conduction): /
QRS (Ventricular conduction): ↑
QT (Ventricular activation to repolarization): ↑
What isthe most important determinant of refractory period in fast channel tissue?
The action potential duration (APD).
What is the most effective drug for ventricular tachycardia and atrial fibrillation but is a drug of last resort because of side effects?
Amiodarone
What are the 2 ways to prevent or terminate sustained tachyarrhythmias such as atrial fibrilation?
- Decreased automatic or DAD arrhythmia (class I agents) by suppressing triggers of re-entry and decrease enhanced automaticity
- Increased refractory period (class III agents) by terminate re-entry
