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CRRAB Week 3 > Adrenergic Agonists > Flashcards

Adrenergic Agonists Flashcards

1
Q

What do you need to know about adrenergic receptors?

A

They are (1) finite (2) specific and (3) bind agonists reversibly

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2
Q

What do sympathetic nerves innervate? What do they cause?

A

Innervate: atria, ventricle, arterioles & veins

Elevate HR, SV & TPR

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3
Q

What is the MAJOR EFFECT of the sympathetic nervous system?

A

Elevate BP

BP = HR x SV x TPR

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4
Q

What is the pathway of NE synthesis? Where does each step occur? What are the enzymes that help out?

A

(1) Tyrosine is converted to DOPA by Tyrosine Hydroxylase [cytosol]
(2) DOPA is converted to Dopamine by DOPA decarboxylase. [cytosol]
(3) Dopamine is converted to Norepinephrine by Dopamine Beta Hydroxylase [Vesicular]
(4) Norepinephrine is converted to Epinephrine by Phenyl-N-methyltransferase [Adrenal medulla]

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5
Q

What is the rate limiting step in the synthesis of adrenergic amines?

A

Tyrosine hydroxylase (first step in cytosol)

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6
Q

What inhibits DOPA decarboxylase?

A

Carbidopa

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7
Q

Where is Dopamine Beta hydroxylse?

A

Intravesicular

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8
Q

Where is Phenyl-N-methyl transferase (PNMT)?

A

Confined to the adrenal medulla (possibly brain; also intravesicular)

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9
Q

What blocks synthesis at tyrosine hydroxylase?

A

Alpha methyl tyrosine (metyrosine)

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10
Q

If someone lacks Tyrosine Hydroxylase, what can they use to produce NE?

A

Dihdroxyphenylserine can be converted to NE by DOPA decarboxylase.

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11
Q

How are adrenergic amines stored?

A
  • In granules with ATP-protein complex
  • 10,000 fold concentration gradient
  • -Axoplasmic uptake (50x concentration gradient)
  • -Granular uptake (200x concentration gradient)
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12
Q

How are adrenergic amines normally released?

A

(1) Induced by stimulation of nicotinic receptors on post-synaptic surface of the post-ganglionic nerve
(2) Depolarization (Na influx) and Ca influx
(3) Release of dopamine beta-hydroxylase, norepinephrine and ATP
(4) NE inhibits its own release (alpha2 receptors)

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13
Q

What are the indirectly-acting sympathomimetics?

A

Ex: tyramine, amphetamine, ephedrine

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14
Q

How do indirectly-acting sympathomimetics act?

A
  • Induce release of NE but not DA beta hydroxylse
  • Reverse direction of axoplasmic catecholamine transporter
  • Characterized by development of tachyphylaxis (desensitization)
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15
Q

When are indirectly acting sympathomimetics (agents releasing catecholamines) inactive?

A

-In the presence of agents that inhibit this axoplasmic pump (Cocaine & Imipramine)

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16
Q

How do Cocaine & Imipramine act?

A

They inhibit the axoplasmic pump to potentiate sympathetic responses.

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17
Q

How does Reserpine act?

A

It inhibits the granular pump accumulating catecholamines in vesicles (results in depletion of catecholamines)

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18
Q

How does Guanethidine and Guanadrel work?

A
  • Induce release from vesicle, probably via displacement
  • Depletes NE stores
  • Reduces response to sympathetic stimulation
  • Slow acting (NE gets degraded by Monoamine oxidase)
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19
Q

When are Guanethidine and Guanadrel inactive?

A

In the presence of inhibitor of the axoplasmic transporter (how Guanethidine gets into cell) or monoamine oxidase inhibitors (what breaks down NE) such as Pargyline or Phenelzine

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20
Q

How to terminate the actions of adrenergic amines?

A

Removal:

  • Uptake processes are of major importance
  • Dilution and diffusion
  • Degradation
  • -COMT (Catechole-O-methyl transferase) (cytoplasm)
  • -MAO (Monoamine oxidase) (mitochondria)
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21
Q

What is COMT? What blocks it?

A

Important in liver for inactivating circulating catecholes

  • Present in all cells
  • Blocked by Tolcapone (Tasmar) - used as adjunct in treatment of Parkinsons
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22
Q

What is MAO?

A

Oxidizes catecholamines

-Two types: a and b

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23
Q

Where are type a and b MAO and what blocks them?

A

Type a - intestine/brain - blocked by perlindole

Type b - various organs - blocked by seligeline & pargyline

24
Q

What can MAO inhibitors do?

A

Ex: Pargyline (Seligeline, Phenylzine..)

-Can potentiate action of catecholamines [may lead to hypertensive crisis]

25
Q

What must individuals taking MAO inhibitors avoid?

A

Foods high in Tyramine (cheese, wine, beer) bc tyramine releases catecholamines and is normally degraded by MAO in intestine. [may lead to hypertensive crisis]

26
Q

When terminating/inactivating adrenergic amines, what is the most predominant urinary product?

A
  • Vanillylmandelic acid (VMA) is predominant urinary product.
  • Normetanephrine is next most common
27
Q

What does alpha1 mediate?

A
  • Smooth muscle contration (primary CV location is blood vessels)
  • Activates phospholipase C (Galphaq dependent process)
  • -To inc. intracellular Ca2+ via inositol trisphosphate
28
Q

What has the most affinity for alpha1?

A

EPI >/= NE&raquo_space; Isoproterenol

29
Q

What does alpha2 mediate?

A
  • Inhibition of neural NE release
  • Prejunctional nerve terminal, platelets, gut, medulla oblongata
  • Acts to decrease cAMP or activate Na/H antiporter
  • -Galphai dependent process
30
Q

What has the most affinity for alpha2?

A

EPI>/= NE&raquo_space; Isoproterenol

31
Q

What does beta1 mediate?

A
  • Adrenergic cardiac effects, inc. HR, renin release
  • Located in heart, JG apparatus & adipose tissue
  • Acts to increase cAMP via Galphas
32
Q

What has the most affinity for beta1?

A

Isoproterenol > EPI = NE

33
Q

What does beta2 mediate?

A
  • Relaxation of smooth muscle & metabolic (glycogenolytic) effects
  • Primary site in CV system is blood vessels (smooth muscle in general)
  • Acts to increase cAMP via Galphas
34
Q

What has the most affinity for beta2?

A

Isoproterenol > EPI&raquo_space; NE

35
Q

What do dopaminergic receptors react with? Where do they act?

A

Dopamine

-Dilation of renal and mesenteric vasculature

36
Q

How can you tell if a drug increases or decreases BP?

A

HR (inc. beta1) x SV (inc. beta1) x R (inc. alpha1)

37
Q

How does Dobutamine act?

A
  • Selective beta1 agonist (actually has vascular activity but net effect is beta1 agonist)
  • Positive inotrope (inc. strength of muscular contraction)
38
Q

What is the therapeutic use and administration of Dobutamine?

A
  • Used for CHF or acute MI with HF
  • Admin: IV
  • Increases BP
39
Q

What is the effect of dopamine?

A
  • CV: positive inotropic (inc. strength of muscular contraction)
  • Beta1
  • Vasodilator in renal and mesenteric vasculature at low doses (dopaminergic)
  • Vasoconstrictor (alpha1) at higher doses
  • Neural: releases NE from nerves
40
Q

How is dopamine administered and what is it used for?

A
  • IV

- Shock - maintains renal perfusion, hypotension - increses bp and CO and chronic refractory heart failure

41
Q

Where does phenylephrine act? What does it do?

A

Alpha1 agonist

  • Used to reverse hypotension or treat paroxysmal atrial tachycardia
  • Also used as decongestant, topical vasoconstrictor, and mydriatic
  • INC. BP
42
Q

What are the largest group of Beta2 selective agonists?

A

Metaproterenol, Terbutaline, Albuterol, Ritodrine, Salmeterol

43
Q

What are beta2 selective agonists used for?

A

Bronchodilation for all except ritodrine [Asthma usually treated with beta2 agonists or glucocorticoids]

44
Q

What drugs are used to delay labor?

A

Beta2 selective agonists:

Ritodrine, Terbutaline

45
Q

What are major side effects of beta2 selective agonists?

A

Tachycardia and palpitations (beta1), tremor (skeletal muscle beta2 stimulation), and headache (beta2 induced vasodilation)

46
Q

What happens to CV system and blood pressure with beta2 selective agents?

A

IV injection - vasodilation of CV (beta2 stimulation)

BP decreases

47
Q

What are the effects of Isoproterenol?

A
  • Vasodilate (beta2)
  • Tachycardia (beta1)
  • Used as a cardiac stimulant (beta1)
  • Decreases BP
48
Q

How is Isoproterenol administered and metabolized?

A

Admin - Parenteral or aerosol

Meta - COMT, not MAO

49
Q

What are the actions of Norepinephrine?

A

Cardio: vasoconstriction (alpha1), Inc. HR & force (beta1), reflex reduction in HR (mediated by vagus nerve)

50
Q

How do you administer NE? What are the contraindications? What do you use it for and what does it do to BP?

A
  • IV
  • Contraindications - Hyperthyroidism, anesthesia, pregnancy
  • Treat hypotension
  • Inc. BP
51
Q

How does EPI act?

A

INC. BP
Cardiovascular - therapeutically usually vasoconstricts (alpha1), can vasodilator (beta2), directly increases HR and force but reflexes to the elevation in blood pressure, can suppress heart rate (vagal stimulation)

52
Q

How is EPI administered?

A

Parenteral, Intraocular or inhaled (300 ug iv for anaphylaxis)

53
Q

How is EPI metabolised?

A

MAO and COMT

54
Q

What are contraindications for EPI?

A

Hyperthyroidism, hypertension, halogen-hydrocarbon anesthetics

55
Q

What are therapeutic uses for EPI?

A
  • Hypersensitivity reactions - low BP and bronchospasm (alpha1 and beta2)
  • With anesthetics (alpha1) - vasoconstriction prevents diffusion of anesthetic, topical hemostatic (alpha1), restore heart beat (beta1)
56
Q

What is the BP equation?

A 
BP = CO x TPR
BP = HR (beta1 - muscarinic) x SV (beta1 - muscarinic) x TPR (alpha1 - muscarinic)

CRRAB Week 3 (12 decks)

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