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Adrenergic Agents (L&J Chp 9) Flashcards

(47 cards)

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1
Q

What are adrenergic agents?

A

Drugs that work on the sympathetic NS

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2
Q

Why do we use adrenergic agents in veterinary medicine?

A

Management of cardiorespiratory function

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3
Q

Sympathomimetics

A
  • Adrenergic ants that stimulate/activate the SNS

- Agonists at a1, b1, b2 R sites; drugs that act at dopamine R sites

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4
Q

Sympatholytics

A

Reduce level of activation of the SNS

-Antagonists at a, b receptors

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5
Q

Classification of sympathomimetics

A
  1. Direct effect at adrenergic R

2. Indirect effect by causing release of NE

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6
Q

Naturally-Occurring Catecholamines

A
  1. Epi
  2. NE
  3. Dopamine
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7
Q

Structure of catecholamines

A
  • Based on benzene ring with various amine side-chains attached at the C1 position
  • If hydroxyl group present at C3 and C4 positions, agent known as catecholamine bc 3,4-dihydroxybenzene AKA catechol
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8
Q

Epinephrine

A

a1, a2, b1, b2
Non-selective, directly acting adrenergic agonist
Primarily used to support CV function during CPR

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9
Q

Storage of epinephrine

A

Light sensitive - colored glass vials, prefilled syringes inside protective packaging

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10
Q

Available formulations of epinephrine

A
  • 0.1mgmL (1:10,000)
  • 1mgmL (1:1000)
  • Also available with local anesthetic solutions for infiltration at concentrations ranging from 1:200,000 to 1:80,000
  • Most formulations contain racemic epinephrine
  • Active form = L-isomer
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11
Q

Administration of epinephrine

A

Systemically by IV injection or via airway during resuscitation (intratracheal administration)
-In humans: also available in metered aerosol preparation to treat swelling associated with upper airway obstruction due to VC effects

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12
Q

What is the active isomer of epinephrine?

A

L-isomer

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13
Q

Where are a1 R located?

A

Smooth Muscle –> BV, bronchi, GIT, urinary, uterus

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14
Q

What is the effect when a1 R are stimulated?

A

CTX of SM, VC

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15
Q

What is the MOA of the a1 R?

A

Excitatory GPCR linked to PLC –> R binding activates PLC –> increased intracellular IP3 –> increased intracellular Ca2+

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16
Q

Where are a2 R located?

A

throughout CNS this is inadequate

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17
Q

What is the effect when a2 R are stimulated?

A
  • Sedation
  • Analgesia
  • Attenuation of sympathetically-mediated responses
  • Platelet aggregation
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18
Q

What is the MOA of the a2 R?

A

Inhibitory GPCR linked to AC –> R binding reduces AC activity –> decrease intracellular [cAMP]

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19
Q

PLC

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A

Phospholipase C

20
Q

IP3

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A

Inositol triphosphate

21
Q

AC

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A

Adenylyl cyclase

22
Q

cAMP

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A

cyclic adenosine monophosphate

23
Q

PKA

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A

Protein kinase A

24
Q

Where are b3 R located?

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A

Adipose tissue

25
What is the effect when b3 R are stimulated?
Lipolysis
26
What is the MOA of the b3 R?
Excitatory GPCR linked to AC: R binding activates AC --> increased intracellular [cAMP]
27
Where are b1 R located?
Heart
28
What is the effect when b1 R are stimulated?
Positive inotropic, chronotropic effects
29
What is the MOA of the b1 R?
Excitatory GPCR linked to AC: binding activates AC --> increased intracellular [cAMP]
30
Where are b2 R located?
Smooth muscle: BV, brooch, GIT, uterus, urinary system; heart
31
What is the effect when b2 R are stimulated?
Relaxation of smooth muscle, vasodilation | Minor positive inotropic, chronotropic effects
32
What is the MOA of the b2 R?
Excitatory GPCR linked to AC: binding to R activates AC --> increased cAMP --> cAMP activates PKA, also increases activity of Na/K ATPase activity which causes hyper polarization
33
Where are dopamine 1 R located?
- Throughout CNS - Vascular SM, kidney - Sympathetic ganglia (etc - WTF is etc?)
34
What is the effect when dopamine 1 R are stimulated?
Modulates extrapyramidal activity | Vasodilation of renal and mesenteric vasculature
35
What is the MOA of the dopamine 1 R?
Excitatory GPCR linked to AC: receptor binding activates AC and leads to an increase in intracellular [cAMP]
36
Where are dopamine 2 R located?
- Throughout CNS - Vascular SM, kidney - Sympathetic ganglia (etc - WTF is etc?)
37
What is the effect when dopamine 2 R are stimulated?
Reduced pituitary hormone output inhibit further noradrenaline release
38
What is the MOA of the dopamine 2 R?
Excitatory GPCR linked to AC: receptor binding reduces AC activity and leads to an decrease in intracellular [cAMP]
39
Epinephrine half-life
-Very short DT rapid metabolism --> necessitates frequent redosing or administration by infusion for a prolonged effect
40
Metabolism of epinephrine
-Following IV admin, rapidly metabolized by mitochondrial monoamine oxidase + catechol-O-methyltransferase within liver, kidney, and circulation to inactive metabolites (3-methoxy-4-hydroxymandelic acid, metanephrine)
41
Excretion of epinephrine
Inactive metabolites (3-methoxy-4-hydroxymandelic acid, metanephrine) conjugated with glucuronic acid or sulfates --> excreted in urine
42
What are the two inactive metabolites of epinephrine?
3-methoxy-4-hydroxymandelic acid | Metanephrine
43
Epi: renal effects
- Causes release of renin from the kidney through multiple mechanisms: stimulation of intrarenal B1 /B2 R, extra renal adrenergic R - Renal blood flow moderately decreased DT regional VC
44
Epi: anesthetic requirements
- Anesthetic requirements related to the release of CNS catecholamines --> predicted that epi will increase MAC of volatile agents - No effect of low-dose epi on MAC of halothane reported in dogs
45
Epi: respiratory effects
- Small increase in minute volume through bronchodilator effects - beta 2 adrenergic R mediated - Pulmonary vascular resistance increased at higher dose rates reflecting agonism at pulmonary vascular alpha 1 adrenergic R
46
Epi: metabolic effects
- Wide-ranging effects that are dose-dependent - Increased basal metabolic rate --> slight increase in body temp following administration - Increased plasma glucose concentrations (multiple mechanisms) - Initial increase in serum K+ followed by hypokalemia followed by increased uptake of K+ into cells (B2 effect)
47
Epi: mechanisms of increased glucose concentrations
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Pharmacology (7 decks)

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