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Pharm II- RCM > Chapter 14 Morgan: Adrenergic Agonist and Antagonist > Flashcards

Chapter 14 Morgan: Adrenergic Agonist and Antagonist Flashcards

1
Q

What is the primary mechanism of action of adrenergic agonists and antagonists?

A
  • They interact with adrenergic receptors (adrenoceptors)
  • To produce clinical effects.
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2
Q

How can the clinical effects of adrenergic drugs be understood?

A
  • By understanding adrenoceptor physiology
  • Knowing which receptors each drug activates or blocks
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3
Q

What are adrenoceptors?

A

Specific receptors that interact with adrenergic agonists and antagonists to mediate their effects.

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4
Q

Why is knowledge of adrenoceptor physiology important in pharmacology?

A

It helps deduce the clinical effects of adrenergic drugs.

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5
Q

What determines the specificity of adrenergic drugs?

A

They activate or block the specific adrenergic receptors.

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6
Q

What is the primary neurotransmitter for adrenergic activity in the sympathetic nervous system?

A

Norepinephrine (noradrenaline).

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7
Q

Where is norepinephrine released in the body, and what are the exceptions?

A

Released by postganglionic sympathetic fibers at end-organ tissues, except in eccrine sweat glands and some blood vessels.

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8
Q

How is norepinephrine synthesized and stored?

A
  • Synthesized in the cytoplasm of sympathetic postganglionic nerve endings.
  • Stored in vesicles.
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9
Q

What terminates norepinephrine’s actions?

A

Primarily terminated by reuptake into the postganglionic nerve ending.

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10
Q

How do tricyclic antidepressants, cocaine, and amphetamines affect adrenergic activity?

A
  • They inhibit transporters that facilitate the removal of norepinephrine from the synapse.
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11
Q

What happens to norepinephrine after it diffuses from receptor sites?

A
  • Is taken up by nonneuronal cells
  • Metabolized by catechol-O-methyltransferase or
  • Metabolized in neurons by monoamine oxidase.
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12
Q

What is the effect of prolonged adrenergic activation?

A
  • Leads to desensitization
  • Reduce responses to subsequent stimulation.
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13
Q

What are the two general categories of adrenergic receptors?

A

1. α (alpha) receptors
2. β (beta) receptors.

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14
Q

How are α and β adrenergic receptors subdivided?

A
  • α receptors into α1and α2
  • β receptors into β1, β2, and β3.
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15
Q

What are the further divisions of α-receptors identified through molecular cloning?

A

α1A, α1B, α1D, α2A, α2B, and α2C.

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16
Q

What is the role of G proteins in adrenergic receptors?

A
  • Are heterotrimeric receptors
  • Linked to different adrenoceptors
  • Each with a unique effector
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17
Q

Which G protein is linked to α1 receptors, and what does it activate?

A
  • Linked to Gq
  • Activates phospholipases
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18
Q

What G protein is α2 receptors linked to?

A
  • Linked to Gi
  • Inhibits adenylate cyclase.
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19
Q

Which G protein is linked with β receptors, and what is its function?

A
  • β is linked to Gs
  • Activates adenylate cyclase.

Includes: β2 β1

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20
Q

Where are α1-Receptors located and what is their primary function?

A
  • Postsynaptic adrenoceptors in smooth muscle throughout the body
  • Increase intracellular calcium ion concentration, causing smooth muscle contraction.
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21
Q

What are the effects of α1-agonists in the body?

A
  • Mydriasis (pupillary dilation)
  • Bronchoconstriction
  • Vasoconstriction
  • Uterine contraction
  • Increase salivation
  • Constriction of gastrointestinal and Genitourinary sphincters.
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22
Q

How does stimulation of α1-receptors affect insulin secretion and lipolysis?

A

Inhibits insulin secretion and lipolysis.

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23
Q

What role do α1-receptors play in the myocardium?

A
  • Possess a positive inotropic effect
  • Might contribute to catecholamine-induced arrhythmia.
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24
Q

How does α1-receptor stimulation affect the cardiovascular system, especially during myocardial ischemia?

A
  • Enhances vasoconstriction
  • Increases peripheral vascular resistance
  • Increases left ventricular afterload
  • Increases arterial blood pressure
  • Enhanced receptor coupling with agonists during myocardial ischemia.
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25
Q

Where are α2-Receptors primarily located, and what is their main function?

A
  • Located on presynaptic nerve terminals
  • It inhibits adenylyl cyclase
  • Reduces calcium ion entry
  • Limits norepinephrine release.
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26
Q

How do α2-Receptors regulate norepinephrine release?

A
  • Create a negative feedback loop
  • Inhibits further norepinephrine release from neurons.
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27
Q

What is the role of postsynaptic α2-Receptors in vascular smooth muscle?

A

Produce vasoconstriction.

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28
Q

How does stimulation of CNS α2-Receptors affect the body?

A
  • Causes sedation
  • Reduces sympathetic outflow
  • Leads to peripheral vasodilation
  • Lower blood pressure.
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29
Q

What are the classifications of β-Adrenergic receptors?

A
  • β1, β2, and β3 receptors.
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30
Q

How do norepinephrine and epinephrine compare in their potency on β1 and β2 receptors?

A
  • Both Equipotent on β1 receptors
  • Epinephrine is more potent on β2 receptors
  • Norepinephrine on β1 receptors.
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31
Q

Where are β1-receptors primarily located, and what is their role in the heart?

A
  • Located on postsynaptic membranes in the heart
  • Stimulate adenylyl cyclase, leading to increased heart rate, conduction, and contractility.
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32
Q

What is the effect of β1-receptor stimulation on cardiac function?

A
  • Activates a kinase phosphorylation cascade
  • Cause positive chronotropic, dromotropic, and inotropic effects.
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33
Q

Where are β2-Receptors primarily located?

A
  • Primarily in smooth muscles
  • Gland cells
  • Ventricular myocytes.
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34
Q

What is the role of β2-Receptors in patients with chronic heart failure?

A

Their contribution to the response to intravenous catecholamines increases in chronic heart failure.

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35
Q

What is the common mechanism of action shared by β2 and β1-Receptors?

A

Both activate adenylyl cyclase.

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36
Q

What are the effects of β2-Receptor stimulation?

A
  • Bronchodilation
  • Vasodilation
  • Relaxation of the uterus, bladder and gut
  • Stimulates glycogenolysis, lipolysis, gluconeogenesis
  • Insulin release
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37
Q

Where are β3-Receptors located?

A
  • Gallbladder.
  • Brain.
  • Adipose tissue.
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38
Q

What is the known role of β3-Receptors in gallbladder physiology?

A
  • Is currently unknown.
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39
Q

What functions are associated with β3-Receptors?

A
  • Play a role in lipolysis
  • Thermogenesis in brown fat
  • Bladder relaxation.
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40
Q

What are Dopamine (DA) receptors?

A
  • A group of dopamine-activated adrenergic receptors
  • Classified as D1 and D2 receptors.
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41
Q

What is the function of D1 receptors?

A

Mediates vasodilation in the kidney, intestine, and heart.

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42
Q

What role do D2 receptors play in medication?

A
  • Involved in the antiemetic action of drugs
  • Like droperidol and haloperidol.
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43
Q

What complicates the prediction of clinical effects of adrenergic agonists?

A
  • Overlapping receptor activity,
  • As epinephrine stimulates α1-, α2-, β1-, and β2-adrenoceptors
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44
Q

How does epinephrine’s net effect on blood pressure vary?

A
  • Depends on dose-dependent balance between
  • α1-vasoconstriction
  • α2- and β2-vasodilation
  • β1-inotropic influences.
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45
Q

What is the distinction between direct and indirect adrenergic agonists?

A
  • Direct agonists bind to receptors.
  • Indirect agonists increase endogenous neurotransmitter activity.
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46
Q

Why is it important to distinguish between direct and indirect agonists?

A
  • Particularly crucial in patients with abnormal endogenous norepinephrine stores
  • Those on some antihypertensive medications
  • Monoamine oxidase inhibitors.
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47
Q

What is unique about the chemical structure of catecholamine adrenergic agonists?

A
  • They have a 3,4-dihydroxybenzene structure
  • Include epinephrine, norepinephrine, and dopamine.
48
Q

How does the modification of side-chain structures in catecholamines affect them?

A
  • Leads to development of synthetic catecholamines
  • Ex: isoproterenol, dobutamine with more receptor specificity.
49
Q

What should be considered when using adrenergic agonist dosing recommendations?

A
  • Recommendations are guidelines only
  • Individual responses to these drugs can vary significantly
50
Q

What is Phenylephrine’s primary effect?

A
  • Peripheral vasoconstriction
  • Increasing systemic vascular resistance
  • Increase blood pressure.
51
Q

How does Phenylephrine affect heart rate?

A
  • Can cause reflex bradycardia
  • Potentially reduce cardiac output.
52
Q

What are some topical uses of Phenylephrine?

A
  • Used as a decongestant
  • Mydriatic agent.
53
Q

How is Phenylephrine administered for reversing hypotension?

A

Intravenous boluses of 50 to 100 mcg (0.5 to 1 mcg/kg).

54
Q

What is the duration of Phenylephrine’s action?

A

Approximately 15 minutes after a single dose.

55
Q

Can tachyphylaxis occur with Phenylephrine infusions?

A

Yes, it may require upward titration of the infusion.

56
Q

How should Phenylephrine be prepared for administration?

A

Diluted from a 1% solution (10 mg/1-mL ampule) to a 100 mcg/mL solution and titrated to effect.

10 mg/mL vial in 100 mL NS bag to get 0.1 mg/mL or 100 mcg/mL

57
Q

What are the effects of Clonidine?

A
  • Decreases anesthetic and analgesic requirements
  • Provides sedation
  • Prolongs the duration of regional anesthesia blocks.
58
Q

What are α2-Agonists commonly used for?

A
  • Antihypertensive effects
  • Negative chronotropic effects
  • Sedation.
59
Q

How does Clonidine affect intraoperative and postoperative management?

A
  • It enhances circulatory stability during surgery
  • Reduces postoperative shivering
  • Helps manage acute pain.
60
Q

What are the side effects of α2-Agonists like Clonidine?

A
  • Bradycardia
  • Hypotension
  • Sedation
  • respiratory depression
  • Dry mouth.
61
Q

How does Dexmedetomidine compare to Clonidine?

A
  • Higher α2-receptor affinity
  • Shorter half-life
  • Stronger α2:α1 receptor specificity ratio.
62
Q

What are the clinical applications of Dexmedetomidine?

A
  • Sedation during awake fiberoptic intubation
  • Postoperative sedation without significant respiratory depression
  • Potential renal protection in ischemic kidney injury.
63
Q

What is the recommended dosing for Dexmedetomidine?

A
  • Loading dose: 1 mcg/kg over 10 minutes,
  • Followed by an infusion of 0.2 to 0.7 mcg/kg/h.
64
Q

What happens upon abrupt discontinuation of long-term α2-Agonists?

A
  • Risk of acute withdrawal syndrome
  • Including hypertensive crisis
65
Q

What is Epinephrine, and where is it synthesized?

A
  • An endogenous catecholamine.
  • Synthesized in the adrenal medulla.
66
Q

How does Epinephrine affect the myocardium?

A
  • Stimulates β1-receptors
  • Raise blood pressure, cardiac output, and myocardial oxygen demand.
67
Q

What is the effect of Epinephrine on α1 and β2 receptors?

A
  • α1: Decreases splanchnic and renal blood flow; increases coronary perfusion.
  • β2: Causes vasodilation in skeletal muscle and relaxes bronchial smooth muscle.
68
Q

What are the primary clinical uses of Epinephrine?

A
  • Treating anaphylaxis.
  • Increasing coronary perfusion pressure during ventricular fibrillation.
69
Q

What are the complications associated with Epinephrine?

A
  • Cerebral hemorrhage
  • Myocardial ischemia
  • Ventricular arrhythmias.
70
Q

How is Epinephrine administered in emergencies?

A
  • Intravenous bolus of 0.5 to 1 mg
  • Anaphylaxis, 100 to 500 mcg followed by infusion.
71
Q

What concentrations of Epinephrine are available?

A
  • 1:1000 (1 mg/mL) vials
  • 1:10,000 (0.1 mg/mL) prefilled syringes.
72
Q

What are the cardiovascular effects of Ephedrine?

A
  • Increases blood pressure
  • Increases heart rate
  • Increases contractility
  • Increases cardiac output
  • Acts a bronchodilator.
73
Q

How does Ephedrine differ from Epinephrine?

A
  • Longer duration
  • Less potency
  • Indirect and direct actions stimulation of CNS
  • Raising of minimum alveolar concentration.
74
Q

What are Ephedrine’s mechanisms of action?

A
  • Peripheral postsynaptic norepinephrine release
  • Inhibition of norepinephrine reuptake.
75
Q

What is Ephedrine’s common use in anesthesia?

A
  • As a vasopressor
  • Especially during hypotension in anesthesia.
76
Q

Why is Ephedrine preferred in obstetric anesthesia?

A
  • It doesn’t decrease uterine blood flow.
  • Now, phenylephrine is often used due to faster onset and fewer fetal pH effects.
77
Q

How is Ephedrine administered?

A
  • Adults: 2.5 to 10 mg bolus.
  • Children: 0.1 mg/kg bolus.
78
Q

What is the cause of Ephedrine’s tachyphylaxis?

A

Likely due to depletion of norepinephrine stores.

79
Q

What are the primary actions of Norepinephrine?

A
  • Direct α1 stimulation
  • Intense vasoconstriction
  • Increased myocardial contractility from β1 effects.
80
Q

What are the effects of Norepinephrine on blood pressure?

A
  • Increases both systolic and diastolic pressures
  • May increase afterload.
81
Q

How does Norepinephrine affect cardiac output?

A
  • Increase afterload
  • Reflex bradycardia
  • May prevent elevation in cardiac output.
82
Q

What concerns are associated with Norepinephrine use?

A
  • Decreased renal and splanchnic blood flow.
  • Increased myocardial oxygen requirements.
83
Q

What is the clinical use of Norepinephrine?

A
  • Management of refractory shock
  • Especially septic shock.
84
Q

How is Norepinephrine administered?

A
  • Continuous infusion
  • Rate of 2 to 20 mcg/min.
85
Q

What is a potential side effect of Norepinephrine infusion?

A
  • Extravasation
  • Tissue necrosis at the infusion site.
86
Q

What are the effects of low doses of Dopamine?

A
  • Activates dopaminergic receptors
  • Dilates renal vasculature
  • Promotes diuresis and natriuresis.
87
Q

How does Dopamine function at moderate doses?

A
  • Stimulates β1 receptors
  • Increases myocardial contractility
  • Increases heart rate
  • Increases systolic blood pressure
  • Increases cardiac output.
88
Q

What occurs at high doses of Dopamine?

A
  • Prominent α1 effects
  • Increased peripheral vascular resistance
  • Decreased renal blood flow.
89
Q

What are Dopamine’s indirect effects?

A

Due to release of norepinephrine from presynaptic sympathetic nerve ganglion.

90
Q

What are the limitations of Dopamine in clinical use?

A
  • Chronotropic and proarrhythmic effects limit its use
  • It has replaced by other drugs in critical illness scenarios.
91
Q

How is Dopamine administered?

A
  • As a continuous infusion
  • Rate of 1 to 20 mcg/kg/min.
92
Q

What type of agonist is Isoproterenol?

A

Is a pure β-agonist.

93
Q

What are the primary effects of β1 stimulation by Isoproterenol?

A
  • Increases heart rate
  • Increase contractility
  • Increase cardiac output.
94
Q

How does Isoproterenol affect systolic and diastolic blood pressure?

A
  • Systolic blood pressure may increase or remain unchanged.
  • β2 stimulation decreases peripheral vascular resistance and lowers diastolic blood pressure.
95
Q

Why is Isoproterenol often not the preferred inotropic choice?

A
  • It increases myocardial oxygen demand
  • Potentially reduce oxygen supply.
96
Q

What receptors does Dobutamine primarily affect?

A
  • Affinity for both β1- and β2-receptors
  • Greater selectivity for β1-receptors.
97
Q

What is the primary cardiovascular effect of Dobutamine?

A
  • Increases cardiac output
  • Due to enhanced myocardial contractility.
98
Q

How does Dobutamine affect peripheral vascular resistance and arterial blood pressure?

A
  • β2 activation leads to decreased PVR
  • Preventing increases in arterial blood pressure.
99
Q

How does Dobutamine impact left ventricular filling pressure and coronary blood flow?

A
  • Decreases LV filling pressure
  • Increases coronary blood flow.
100
Q

Should Dobutamine be used routinely for myocardial oxygen consumption?

A
  • No, it increases myocardial oxygen consumption
  • Is not recommended for routine use without specific indications.
101
Q

In what clinical scenario is Dobutamine commonly used?

A

It is often employed in pharmacological stress testing.

102
Q

How is Dobutamine typically administered?

A
  • Administered as an infusion
  • Rate of 2 to 20 mcg/kg/min.
103
Q

What type of receptor agonist is Fenoldopam, and what is its primary action?

A
  • Selective D1-receptor agonist
  • Decreases PVR
  • Increases renal blood flow.
104
Q

In which surgical scenarios is Fenoldopam commonly used?

A
  • Used in cardiac surgery
  • Aortic aneurysm repair
  • Potential risk of perioperative kidney impairment.
105
Q

What are the key clinical indications of Fenoldopam?

A
  • Severe hypertension
  • Particularly in patients with renal impairment
  • PreventS contrast media-induced nephropathy.
106
Q

How is Fenoldopam administered and titrated?

A
  • Continuous infusion of 0.1 mcg/kg/min
  • Increments of 0.1 mcg/kg/min at 15- to 20-minute intervals
  • Until the target blood pressure is achieved.
107
Q

What are the effects of Fenoldopam on renal function and blood pressure?

A
  • It reduces blood pressure
  • Helps to maintain renal blood flow.
108
Q

Is there strong evidence supporting Fenoldopam’s renal protection efficacy?

A
  • The efficacy of Fenoldopam in “protecting” the kidney perioperatively remains debated
  • No strong evidence for efficacy.
109
Q

What is a notable side effect of lower doses of Fenoldopam?

A
  • Associated with less reflex tachycardia.
110
Q

The term adrenergic originally referred to:

A
  • The effects of Epinephrine
    (adrenaline)
111
Q

What is the primary neurotransmitter responsible for most of the adrenergic activity of the sympathetic nervous system?

A

Norepinephrine (Noradrenaline)

112
Q

Where can Dopamine be converted into Epinephrine?

A

In the Adrenal Medulla

113
Q

Monoamine oxidase (MAO) And catechol-O-methyltransferase (COMT) produces a common end product known as:

A

Vanillylmandelic acid (VMA).

114
Q

What are the naturally
occurring catecholamines?

Think about END

A
  • Epinephrine
  • Norepinephrine
  • Dopamine (DA)
115
Q

Adrenergic Agonists that have a 3,4-
dihydroxybenzene structure and are known as:

A
  • catecholamines.
  • These drugs are typically short-acting because of their metabolism by monoamine oxidase and catechol-O-methyltransferase
116
Q

Which drugs are synthetic catecholamines?

A
  • Isoproterenol
  • Dobutamine

Tend to be more receptor-specific

Pharm II- RCM (2 decks)

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