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Pharmacology > Adrenergic Agonists > Flashcards

Adrenergic Agonists Flashcards

1
Q

What can we do with these drugs to have a more profound effect?

A

Use with an anticholinergic

ex- B agonist to treat asthma (bronchodilation), anticholinergic (blocks bronchocontriction –> bronchodilation)

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2
Q

How are adrenergic agonists inactivated?

A

reuptake

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3
Q

What pathway is alpha-1 receptors coupled to?

A

Gq

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4
Q

Where are alpha-1 receptors located?

A
  • radial muscles
  • blood vessels in skin and splanchnic vessels
  • GI/bladder (sphinctors)
  • GI wall (relaxation)
  • Salivary glands (incr secretion slightly)
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5
Q

Adrenergic agonists are useful for hypotension, but what what can overstim cause and why?

A

hemorrhage because of incr bp

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6
Q

Pure alpha-1 agonists cause incr bp and reflex bradycardia. Which drugs will block this reflex?

A

Ganglionic blockers like hexamethonium.

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7
Q

Where are alpha-2 receptors?

A
  • presyn (autoregulatory)
  • pancreas (inh insulin release)
  • present post-syn where they cause vasoconstriction if given by IV
  • CNS (stim of these decr symp outflow)
  • ciliary body (inh aq humor production)
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8
Q

Where are B-1 receptors located?

A
  • Heart (incr HR, incr FOC, incr conduction)
  • Kidney (incr renin)
  • Eye (incr aq humor production)
  • Salivary glands (incr amylase secretion)
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9
Q

What are B receptors coupled to?

A

Gs

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10
Q

What are alpha-2 receptors coupled to?

A

Gi

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11
Q

Where are B-2 receptors located?

A
  • ciliary body (relax- contract lens so sq humor can escape
  • Bronchi (relax)
  • Blood vessels in muscle (relax)
  • GI/bladder wall- detrusor (relax)
  • Liver (incr glu)
  • Pancreas (incr insulin)
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12
Q

What are B-2 agonists used for clinically?

A

asthma and to prolong labor

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13
Q

Since B-2 agonists lead to incr cAMP, what does that lead to?

A

leads to phosphorylation, then inh myosin light chain kinase

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14
Q

What does it mean if the diastolic and systolic peaks in a HR are close together?

A

The heart is beating faster

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15
Q

What does it mean if the pulse width is increased?

A

increased strength of contraction

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16
Q

When does the stimulation of the eccrine sweat glands do? And where are eccrine glands located?

A

causes generalized sweating

-located all over the body but mostly palms and soles of feet

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17
Q

What happens when adrenergic get into the CNS?

A
  • They don’t normally get in but they can with a high conc

- Cause adrenaline rush or feeling of disaster, and arousal, euphoria, anorexia

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18
Q

Why don’t we prefer to use symp drug for shock?

A
  • the usual treatment is volume replacement via IV. The goal is to maintain tissue perfusion, not necessarily bp.
  • so with symp drugs, too much vasoconstriction can hinder organ perfusion.
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19
Q

What are 3 drugs we can possible use for shock and why?

A

dopamine- when heart needs to be stim and there is low bp

dobutamine- if bp isn’t necessarily an issue. It has less effect on oxygen demand bc it works exclusively on FOC

NE- if bp is low

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20
Q

Acute hypotension

A
  • best treatment is to lie patient down because that will incr bp, and also give fluids.
  • don’t use vasoconstrictive agent if no immediate threat
21
Q

What would you give for orthostatic hypotension?

A

alpha-1 agonist

22
Q

What is heart block, and which drugs would and wouldn’t you use?

A
  • heart block is when electrical signal causing heart to contract and pump blood is slowed or disrupted.
  • epi has been used
  • but pacemaker should be inserted ASAP
  • isoproterenol NOT good because it incr cardiac work
23
Q

Low dose epi

A
  • B receptors

- incr HR, decr bp

24
Q

Med dose epi

A
  • B receptors, and moderate effect on alpha

- since alpha-1 incr bp and beta-2 dec bp it balances out to med incr in bp

25
Q

high dose epi

A
  • alpha-1

- response looks like norepi

26
Q

What can epi cause?

A

-hyperglycemia bc incr glu (B2) and inh insulin (alpha-2)

27
Q

What is epi used for clinically?

A

anaphylactic shock, cardiac arrest (B1), reduce bleeding during surgery, prolong actions of local anesthetics

28
Q

What is the good coordinated effect of epi with glu?

A

first stim alpha-2 to inh insulin causing large amts of glu, the beta-2 cause modest incr in insulin to use the glucose.

29
Q

Norepi

A
  • doesn’t activate B2, activates alpha-1, alpha-2 and beta-1
  • behaves like alpha agonist
  • vasoconstriction (alpha1)- used for hypotension and shock if bp is low
  • direct acting adrenergic agonist
30
Q

Dopamine

A

D receptors- vasodilation in kidney

  • inotropic effect on the heart
  • used for cardiogenic and non cardiogenic shock
  • direct acting adrenergic agonist
31
Q

phenylepherine

A
  • alpha-1 agonist
  • cause vasoconstriction, incr bp and mydriasis
  • used as nasal decongestant, mydriasis w/o cycloplegia (tropicamide will), terminate paroxysmal tach (baro reflex), hypotension
  • cannot be converted to meth
32
Q

methoxamine

A
  • alpha-1 agonist

- used for orthostatic hypotension and paroxysmal tachy

33
Q

clonidine

A
  • alpha-2 agonist
  • decr bp
  • but incr bp at high doses
34
Q

methyldopa

A
  • alpha 2 agonist

- decr bp

35
Q

dobutamine

A
  • beta-1 agonist
  • treats cardiogenic shock – if bp isn’t an issue, less effect on oxygen demand bc only B1 (no vasoconstriction_
  • treats acute heart failure
  • used in patients with low cardiac output basically because it stimulates the heart
  • it’s an inotrope (incr strength of contraction)
36
Q

albuterol

A
  • b-2 agonist

- for asthma

37
Q

salmeterol

A
  • B2 agonist

- used for asthma and premature labor (bc B2 for uterine relaxation)

38
Q

tertbutaline

A
  • B2 agonist

- used for asthma and premature labor (bc B2 for uterine relaxation)

39
Q

ritodrine

A
  • B2 agonist

- used for asthma and premature labor (bc B2 for uterine relaxation)

40
Q

metaproterenol

A
  • b-2 agonist

- for asthma

41
Q

Isoproterenol

A
  • B1 and B2 agonist
  • similar to low dose of epi
  • has been used for asthma,bronchospasm, heart block and arrythmias
  • not agent of choice for any application
42
Q

mixed acting sympathomimetics

A

-stimulate the receptor but also causes NT release

43
Q

ephedrine

A
  • mixed acting adrenergic agonist
  • causes release of NE
  • component of herbal med
  • degongestant (main), bronchospasm, hypotension
44
Q

pseudoephedrine

A

-mixed acting adrenergic agonist
degongestant (main), bronchospasm, hypotension
-can be used to make meth

45
Q

indirect acting sympathomimetics

A

-only work by causing the release of a NT, has no effect on the receptor

46
Q

cocaine

A
  • indirect acting adrenergic agonist
  • blocks NE and dopamine reuptake
  • analogues used for local anesthesia
47
Q

amphetamine

A
  • indirect acting adrenergic agonist
  • stimulant
  • treats ADHD and narcolepse
  • incr NE and dopamine release
48
Q

Tyramine

A
  • indirect acting adrenergic agonist
  • not a drug, component of food
  • some drugs (MAOI) inh tyramine deg enzyme – causes hypertensive emergency and large amounts can enter CNS

Pharmacology (10 decks)

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