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Adrenergic Agonists and Antagonists Flashcards

1
Q

Epinephrine’s dose dependent effect on different adrenoceptors

A

Functions as a hormone - acts on distant cells after release from adrenal medulla

Agonist at both a and b receptors

At low concentrations: epinephrine activates mainly b1 and b2 receptors

At higher concentrations, a1 effects become more pronounced

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2
Q

Effects of epinephrine at physiological doses

A

Increases heart rate and force of contradiction (b1). Cardiac output increases = oxygen demand of the myocardium increases

Increased renin release (b1)

Increased lipolysis (b1 and b2 effect)

Constricts arterioles in skin and viscera (a1)

Dilates blood vessels of skeletal muscle (b2)

Relaxes bronchial smooth muscle (b2)

Increases liver glycogenolysis

Increased glucagon release from a cells of pancreas (b2)

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3
Q

Effect of epinephrine on blood pressure when given IV in large doses vs low doses

A

Large dose: increase in MAP

  • Increased ventricular contraction (b1) –> increased systolic
  • Increased heart rate (b1) –> this may be opposed by the baroreceptor reflex
  • Vasoconstriction (a1) –> increased diastolic

Small dose: no change in MAP

  • Peripheral vascular resistance decreases due to vasodilation as b2 receptors are more sensitive to epinephrine than a1 –> fall in diastolic
  • Increased contractility due to b1 –> systolic increases
  • Heart rate increases (b1 effect) –> no change in blood pressure so baroreceptor reflex does not kick in
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4
Q

Uses of epinephrine

A

DOC for anaphylactic shock

Acute asthmatic attacks

Cardiac arrest

In local anesthetics: epinephrine increases duration of local anesthesia by producing vasoconstriction at teh site of injection

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5
Q

Norepinephrine specificity to adrenoceptors

A

Agonist at a1, a2 and b1 receptors

Little action on b2 receptors

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6
Q

Cardiovascular effects of IV infusion of norepinephrine

A

Peripheral vasoconstriction (a1)

Increases cardiac contractility (b1)

Increases PVR, systolic pressure and diastolic pressure –> increase in MAP –> triggers baroreceptor reflex –> reflex bradycardia

Cardiac output unchanged or decreases

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7
Q

Uses of norepinephrine

A

To treat shock because it increases vascular resistance and blood pressure

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8
Q

Baroreceptor reflex in response to increase in blood pressure

A

Baroreceptors in carotid sinus are mechanoreceptors that sense changes in blood pressure

1) Inhibits sympathetic activity at –> decrease force of contraction of heart (decreased activation of b1)
2) Stimulates parasympathetic activity –> Decreases heart rate (activation of m2 in atria)

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9
Q

Baroreceptor reflex in response to decrease in blood pressure

A

1) Stimulate sympathetic activity –> increase in force of contraction of heart
2) Inhibit parasympathetic activity –> increase in heart rate (inhibition of m2 receptors in atria)

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10
Q

Effect of atropine pre-treatment + norepinephrine on CVS

A

If atropine is given first, it will block the muscarinic receptors and block the baroreceptor reflex

So norepinephrine will cause increase in PVR, vasoconstriction and increased force of contraction which will increase MAP –> tachycardia

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11
Q

Dopamine selectivity for adrenoceptors

A

Dose dependent activation of a and b receptors. Physiologically activates D1 but in therapeutic doses can activate a1 and b1 too.

D1 > b1 > a1

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12
Q

Cardiovascular effects of low, intermediate and high rates of dopamine infusion

A 
Low rate infusion:
Activates D1 receptors in renal and other vascular beds leading to:
- Vasodilation 
- Increased GFR 
- Increase in renal blood flow 
- Increase in sodium excretion 
Intermediate rate of infusion 
Dopamine activates b1 receptors in heart and causes release of NE from nerve terminals which leads to:
- Increased cardiac output 
- Increased systolic BP
- Unchanged diastolic BP 
- Increased in MAP 
- PVR unchanged 
High rate of infusion:
Dopamine activates vascular a1 receptors:
- Vasoconstriction 
- Increased PVR 
- Increased MAP
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13
Q

Dopamine uses (2)

A

Treatment of severe CHF

Treatment of cariogenic and septic shock
–> Intermediate to high rates of infusion are used to activate b1 and a1 receptors

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14
Q

Fenoldopam MOA and uses

A

D1-receptor selective agonist –> peripheral vasodilation in some vascular beds.

Indicated for in-hospital, short-term management of severe hypertension.

Fenoldopam should be administered by continuous intravenous infusion. A bolus dose should not be used.

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15
Q

Isoproterenol MOA and cardiovascular effects

A

Non-selective b-adrenergic agonist –> activates b1 and b2 receptors

Bronchodilation (b2)

Increases force of contraction and cardiac output (b1) –> systolic BP remains unchanged or rises

Dilates arterioles of skeletal muscle (b2) –> decrease in PVR –> diastolic BP falls

MAP typically falls –> increase in heart rate due to reflex tachycardia

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16
Q

Isoproterenol uses

A

Used in emergencies to stimulate heart rate in patients with bradycardia or heart block

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17
Q

Dobutamine MOA and cardiovascular effects

A

Predominantly b1 agonist

Increases force of contraction very well but has mild effect on heart rate.

Increases myocardial oxygen consumption therefore can be used for the dobutamine stress EKG

Causes mild vasodilation –> small decrease in PVR –> small increase in HR

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18
Q

Dobutamine uses (3)

A

Management of acute heart failure

Management of cardiogenic shock

Used in the dobutamine stress echocardiogram

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19
Q

Albuterol MOA and uses

A

Short acting b2 agonist –> bronchodilator

Management of acute asthma symptoms

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20
Q

Salmeterol and formoterol MOA and uses

A

Long acting b2 agonist –> bronchodilator

Prolonged duration of action (12 hours) due to very high lipid solubility –> slow onset of action

Used in asthma and COPD but cannot be used for prompt relief of acute symptoms

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21
Q

Albuterol, salmeterol and formoterol AE

A

b2 agonists

Tremor, restlessness, apprehension, anxiety

Yes are less likely with inhalation therapy than with parenteral or oral therapy

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22
Q

Phenylephrine MOA, cardiovascular effects

A

a1 agonist

Vasoconstriction –> large increase in PVR –> increased MAP –> reflex bradycardia

Decrease volume of nasal mucosa by decreasing resistance to airflow

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23
Q

Phenylephrine uses

A

a1 agonist

Nasal decongestant: given orally or topically

Mydriasis (but no cycloplegia)

Used to increase BP in hypotension resulting from vasodilation in septic shock or anaesthesia

Used to increase BP and terminate episodes of supra ventricular tachycardia

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24
Q

Clonidine MOA and cardiovascular effects of IV vs oral infusion, AE

A

Partial a2 agonist

Centrally acting antihypertensive

Activates central presynaptic a2 receptors –> reduces release of catecholamines –> reduces sympathetic outflow –> reduces blood pressure

IV infusion of clonidine causes an acute rise in blood pressure, because of activation of postsynaptic a2 adrenoceptors in vascular smooth muscle. This transient vasoconstriction is followed by a more prolonged hypotensive response which results from decreased sympathetic outflow from the CNS. The hypertensive response that follows IV administration is not seen when the drug is given orally.

AE: lethargy, sedation, xerostomia

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25
Methyldopa MOA, effects, uses and AE
Taken up by noradrenergic neutrons --> converted to a-methynorepinephrine --> activates central a2 receptors Decreases blood pressure DOC for treatment of hypertension in pregnancy AE: sedation, impaired mental concentration and xerostomia
26
Brimonidine MOA and uses
Highly selective a2 agonist Given ocularly to lower intraocular pressure in glaucoma Reduces aqueous humour production and increases outflow
27
Amphetemine MOA, effect and uses
Releasing agent --> displaces endogenous catecholamines from storage vesicles Has central stimulatory action Can increase blood pressure (a agonist action of vasculature) and b-stimulatory effects on heart Marked behavioral effects including increased alertness, decreased fatigue, depressed appetite, and insomnia Used to treat ADHD and narcolepsy
28
Methyphenidate MOA, effect and uses
Structural analog of amphetamine Releasing agent --> displaces endogenous catecholamines from storage vesicles Has central stimulatory action Used to treat ADHD in children
29
Tyramine contraindications
Found in fermented foods such as ripe cheese and Chianti wine Normally oxidised by MOA If the patient is taking MAO inhibitors, it can precipitate serious vasopressor episodes.
30
Cocaine MOA
Blocks monoamine reuptake into presynaptic terminals. Most potent at blocking the dopamine transporter (DAT); higher concentrations block the serotonin transporter (SERT) and the norepinephrine transporter (NET). This blockade leads to accumulation of the monoamines in the synaptic space resulting in potentiation and prolongation of their central and peripheral actions.
31
Cocaine effects
The sympathetic effects of cocaine include tachycardia, hypertension, pupillary dilation and peripheral vasoconstriction. The major action of cocaine in the CNS is the inhibition of dopamine reuptake into neurons of the pleasure centers (the limbic system) of the brain --> this produces the intense euphoria
32
Atomoxetine MOA and use
Selective inhibitor of norepinephrine reuptake transporter Used for treatment of ADHD
33
Modafinil MOA and use
Psychostimulant --> inhibitors norepinephrine and dopamine transporters --> increases synaptic concentrations of NE, dopamine, serotonin and glutamate and decreases GABA levels Used for treatment of narcolepsy
34
Ephedrine MOA and PK
Mixed acting adrenergic agonists --> induce NE release and active adrenergic receptors Not a catecholamine - poor substate for COMT and MOA --> long duration of action Penetrates CNS and good oral absorption
35
Ephedrine uses
Mixed acting adrenergic agonist Uses are pressor agent --> especially during spinal anesthesia Used as adjunct in myasthenia gravis
36
Pseudoephredine MOA and uses
Mixed acting adrenergic agonists --> induce NE release and active adrenergic receptors One of four ephedine enantiomers Available OTC as a component of many decongestant mixtures
37
Non-selective a antagonists
Phenoxybenzamine - irreversible | Phentolamine - reversible
38
a1 selective antagonists
Prazosin Terazosin Doxazosin Tamsulosin
39
Non-selective b blockers
Propanolol Nadolol Timolol
40
b1 selective antagonist
Atenolol Metoprolol Esmolol
41
a1 and b-antagonists
Labetalol | Carvedilol
42
Partial b-agonist
Pindolol
43
Inhibitor of NE synthesis
Metyrosine - competitive inhibitor of tyrosine hydroxylase
44
Inhibitors of NE storage
Reserpine --> Irreversibly blocks VMAT | Tetrabenazine --> Reversibly blocks VMAT
45
Phenoxybenzamine MOA, uses
Irreversible non-selective a-agonist Unsuccessful for HTN: Blocks a2 which are found pre-synaptically --> increases catecholamine release. Prevent vasoconstriction --> decreased PVR --> reflex tachycardia Used in pheochromocytoma - prior to surgical removal - for chronic management of inoperable tumors
46
Phentolamine MOA and contraindications
Reversible non-selective a-agonist Causes postural hypotension. Phentolamine-induced reflex cardiac stimulation and tachycardia are mediated by the baroreceptor reflex and by blocking the a2-receptors of the cardiac sympathetic nerves. Contraindicated in patients with decreased coronary perfusion.
47
Phentolamine Uses (4)
Pheochromocytoma - control of hypertension during prep preparation and surgical excision Diagnosis of pheochromocytoma - phentolamine blocking test Prevention of dermal necrosis after extravasation of NE Hypertensive crisis due to stimulant drug overdose (Cocaine, methamphetamines, MOA inhibitors + tyramine ingestion)
48
CVS effects of prazosin, terazosin, doxazaosin, tamsulosin
a1 selective blockers Lower arterial BP by relaxing both arterial and venous smooth muscle First dose produces an exaggerated hypotensive response that can result in syncope First dose must be 1/3 or 1/4 of normal dose
49
a1 blockers uses
Hypertension --> but not DOC DOC for symptom relief from BPH --> relaxation of smooth muscle in bladder neck, prostate capsule and prostatic urethra --> improved urinary flow
50
Tamsulosin MOA
Selective antagonist of a1A receptors that predominate in GU smooth muscle Approved for BPH Little effect on BP and less likely to cause orthostatic hypertension
51
Uses of b-adrenergic antagonists
Hypertension - lower BP by decreasing cardiac output Glaucoma - Decrease aqueous humor secretion. Decreased IOP (Timolol) Migraine - effective for prophylaxis of migraine Hyperthyroidism Angina Pectoris - decrease the O2 requirement of the heart muscle --> reduce chest main on exertion. Contraindicated in variant angina Atrial Fibrillation - control ventricular rate MI - protective effect on myocardium Performance Anxiety Essential tremor
52
Non-selective b-blockers effects on CVS, lungs and metabolism
Propanolol Nadolol Timolol CVS: - Slow heart rate and decrease myocardial contractility - Reduction in cardiac output - Reduction of renin release from the juxtaglomerular cells of the kidney - A central action, reducing sympathetic activity - b-blockers don’t induce postural hypotension because a1-adrenoceptors remain unblocked, therefore, normal sympathetic control of the vasculature is maintained Lungs: blocking b2 can precipitate respiratory crisis in patients with COPD or asthma (causes bronchoconstriction) Metabolic effects: - Decreased glycogenolysis - Decreased glucagon secretion
53
Contraindication of non-selective b-blockers
Asthma patients If an insulin-dependent diabetic is to be given propranolol, very careful monitoring of glucose is essential, since pronounced hypoglycemia may occur after insulin injection and if it occurs, the symptoms of hypoglycemia will be masked
54
b1 selective antagonists uses
Atenolol Metoprolol - useful in hypertensive patients with impaired pulmonary function - useful in diabetic hypertensive patients who are receiving insulin or oral hypoglycemic agents Esmolol - ultra-short acting - given IV for rapid control of ventricular rate in patients with atrial fibrillation or atrial flutter
55
Labetalol and carvedilol MOA and uses
Competitive a1 and b antagonists (more potent as a b-antagonist) Labetalol - used in HTN Carvedilol - used in HTN and CHF, has antioxidant properties
56
Pindolol MOA and uses
Partial b-agonist B-blockers with partial agonist activity may produce smaller reductions in resting heart rate and blood pressure. May be preferred as antihypertensive agents in individuals with diminished cardiac reserve or a propensity to bradycardia
57
b-blockers AE
Non-selective b-blockers: - Bronchoconstriction - Hypoglycemia Lipid metabolism: - Inhibits release of free FAs from adipose tissue - Increase TG and reduce HDL CNS effects: - Sedation - Dizziness - Lethargy - Fatigue
58
Precautions when giving b-blockers
Should not be withdrawn abruptly (especially in patients with CAD) Gradually tapered to avoid acute tachycardia, hypertension and/or schema AE are due to up regulation of b-receptors
59
a-methyltyrosine MOA and uses
Competitive inhibitor of tyrosine hydroxylase --> inhibitor of NE synthesis Used for management of malignant pheochromocytoma Used pre-op before resection of pheochromocytoma
60
Reserpine MOA and uses
Irreversible blocks VMAT --> vesicles cannot store NE or dopamine --> depletion of NE Gradual decrease in blood pressure and decreased HR --> slow onset but long duration of action Used in the past to treat HTN
61
Tetrabenazine MOA and use
Reversible inhibitor of VMAT --> vesicles cannot store NE or dopamine Treatment of chorea associated with Huntington's Disease

Pharmacology (20 decks)

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