Adrenergic Agonists / Antagonists Flashcards
Adrenergic agonists are also referred as?
Sympathomimetics
Adrenergic agonists bind to what receptors?
Adrenergic Receptors
Drugs can activate adrenergic receptors by 4 basic mechanisms
Direct receptor binding
Promotion of Norepinephrine release
Inhibition of Norepinephrine reuptake
Inhibition of Norepinephrine inactivation
Direct receptor binding - three natural transmitters.
drugs activate peripheral adrenergic receptors. Mimics the action of natural transmitters (Norepinephrine, epinephrine and dopamine).
Promotion of Norepinephrine Release
Acting on terminals of sympathetic nerves to cause NE release, drugs can bring about indirect activation of adrenergic receptors.
Amphetamines and cocaine work this way –drugs cause NE release in the synapses but they don’t bind directly to receptors
Inhibition of Norepinephrine reuptake
Blocking NE reuptake, drugs can cause NE to accumulate within the synaptic gap
This action increases receptor activity
Cocaine and tricyclic antidepressants have the ability to block NE reuptake
Inhibition of Norepinephrine inactivation
Some of the NE in nerve terminals of adrenergic neurons undergoes inactivation by monoamine oxidase (MAO)
Drugs that inhibit MAO can increase the amount of NE available for release, and enhance receptor activation
MAO inhibitors are used to treat depression
A1 Agonists - two main responses
Vasoconstriction in blood vessels of the skin, viscera, and mucous membranes
Mydriasis of the eye
Indications for A1 Agonist use and examples
Alpha 1 agonists are given to stop bleeding, primarily in the skin and mucous membranes
Epinephrine, applied topically is the alpha 1 agonist used most often for this purpose
Nasal congestion results from dilation and engorgement of blood vessels in the nasal mucosa
A1 stimulating drugs can relieve congestion by causing alpha 1 mediated vasoconstriction
Phenylephrine and pseudoephedrine are examples
Why is A1 Agonist combined with local anesthetics and what happens / where
To delay systemic absorption
Vasoconstriction reduces blood flow to the site of anesthetic administration
This is done to keep the drug at the local site of action to prolong anesthesia (LET –lidocaine, epinephrine, tetracaine)
A1 Agonist on BP
Elevation of BP: A1 agonists can elevate blood pressure in hypotensive patients
They are typically used in patients where fluid replacement is contraindicated, or when fluid replacement has failed to restore adequate pressure (multiple fluid boluses)
Adverse Effects of A1 Activation three effects
Hypertension: A1 receptor activation can easily cause HTN, especially with IV vasopressors
Necrosis: If IV lines used to infuse A1 agonists become extravasated (interstitial) A1 agonists can easily cause tissue death
Bradycardia: A1 agonists can cause a reflex which slows the heart (increase in BP→ baroreceptor reflex)
A2 Agonists - Location, activation and when should it not be used?
A2 receptors are located presynaptically, and their activation inhibits NE release
Several adrenergic agonists (Epi & NE) are capable of causing A2 activation
There are no therapeutic applications of A2 activation in the peripheral nervous system
What two effects are produced by A2
- Reduction of sympathetic outflow to the heart and blood vessels
- Relief of severe pain
Clonidine is an example of an alpha 2 agonist that causes receptor activation in the CNS. This drug reduces sympathetic tone to blood vessels and to the heart (HTN)
B1 Agonists use in HF / Shock
B1 agonists are useful in the following conditions:
Heart failure: activation of b1 receptors in the heart has positive inotropic effects and activation can improve cardiac performance
Shock: B1 agonists are able to maintain blood flow to vital organs by increasing chronotropic & inotropic effects
B1 effects on AV heart block and Cardiac Arrest
Atrioventricular heart block: activation of cardiac b 1 receptors can enhance impulse conduction through the AV node
Cardiac arrest: by activating cardiac b1 receptors drugs can initiate contraction of the heart
B1 Agonist Adverse Effects
Overstimulation of cardiac b1 receptors can produce tachycardia and dysrhythmias
Angina pectoris: increasing the workload on the heart (making it pump harder and faster) can induce chest pain due to atherosclerosis. B1 agonists increase cardiac oxygen demand
B2 Agonists - Location, Receptor activation, promotes and why selective b2 agonists are preferred plus an example.
B2 activation is limited to the lungs and uterus
B2 receptor activation is primarily used to treat asthma, and other forms of bronchospasm
B2 activation promotes bronchodilation
B2 selective agonists are preferred (Ventolin), because they will not increase cardiac workload (B1 effects)
Isoproterenol
Isoproterenol is a drug which is not beta selective
It will activate B1 and B2 receptors, therefore it is not as desirable for patients with a cardiac history
Delay of preterm labour: by activating B2 receptors in the uterus, smooth uterine muscle relaxes and this has the ability to delay preterm labour
Adrenergic Antagonists block what receptors?
Adrenergic antagonists cause direct blockade of adrenergic receptors
Nearly all cause reversible(competitive) blockade
Alpha Receptor Antagonists - A1 and A2 blockers are not commonly used in EMS; give examples and why they are used.
A1 and A2 blockers are not commonly used in EMS services
An example of a non selective alpha blocker is Phentolamine. This drug can block A1 and A2 receptors
It’s uses include: prevention of tissue necrosis following extravasation of IV A1 blockers, and reversal of soft tissue anesthesia
Beta Receptor Antagonists - Common Beta 1 blockers examples and three benefits
B1 blockers include metoprolol, labetalol, bisoprolol, atenolol, and esmolol
3 major benefits of B1 blockade are: reduced heart rate, reduced force of contraction, and reduced velocity of impulse conduction through the AV node
Beta Receptor Antagonists - How are Beta 1 blockers commonly used to control high heart rates (atrial fibrillation/atrial flutter)?
Beta 1 blockers are commonly used to control high heart rates (atrial fibrillation/atrial flutter)
By blocking B1 receptors in the heart:
- Rate of sinus nodal discharge is decreased
- Conduction of atrial impulses through the AV node is slowed
Beta Receptor Antagonists Other non EMS uses include:
Treatment of angina Treatment of HTN Treatment of MI Treatment of heart failure Treatment of Phenochromocytoma
