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: ++