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Adrenergics Flashcards

1
Q

What is an a1 specific adrenergic agonist?

A

phenylephrine

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2
Q

What is an a2 specific adrenergic agonist?

A

clonidine

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3
Q

What are the four b2 specific agonists?

A

(STARs for asthma)

  1. salmeterol
  2. terbutaline
  3. albuterol
  4. ritodrine
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4
Q

What are the b1 specific agonists?

A

dobutamine

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5
Q

What are the beta adrenergic agonists (not specific for 1 or 2)?

A

isoproterenol

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6
Q

What receptors do dopamine stimulate?

A

D1>b1>a1

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7
Q

What are the four INDIRECTLY acting adrenergic agonists?

A

(indirect drugs are TAME)

  1. tyramine
  2. amphetamine
  3. ephedrine
  4. methylphenidate
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8
Q

What are the inhibitors of neuronal uptake of biogenic amines (NE specifically)?

A

cocaine and tricyclic antidepressants

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9
Q

What are the agents that interfere with adrenergic nerve function?

A

methyldopa and reserpine

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10
Q

What are the alpha-adrenergic ANTAGONISTs?

Do they have specificity to specific a receptors?

A

phenoxybenzamine (a1, a2)
prazosin (a1)
tamsulosin (a1)

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11
Q

What are the beta-adrenergic ANTAGONISTs?

What is their specificity to b1 or b2?

A

propanolol (b2,b1)
metoprolol (b1)
atenolol (b1)

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12
Q

What adrenergic antagonist effects b and a1 receptors?

A

carvedilol

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13
Q
  1. What are the locations of a1 receptors?
  2. What is their function?
  3. What type of G protein?
  4. Agonist?
  5. Antagonist?
A 
1. vasculature- contract
smooth muscle- contract
liver- glycogenolysis
glands-secrete
3. Gq (increased Ca)
4. phenylephrine
5. prazosin
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14
Q
  1. What are the locations of a2 receptors?
  2. What is their function?
  3. What type of G protein?
  4. Agonist?
  5. Antagonist?
A
  1. presynaptic terminal- inhibit further release
    pancreatic islets- inhibition of secretion
  2. Gi/o (decrease cAMP, CA and increase K)
  3. clonidine
  4. n/a
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15
Q
  1. What are the locations of b1 receptors?
  2. What is their function?
  3. What type of G protein?
  4. Agonist?
  5. Antagonist?
A
  1. heart- increase contractility and HR
  2. Gs (increase AC)
  3. dobutamine
  4. metoprolol
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16
Q
  1. What are the locations of b2 receptors?
  2. What is their function?
  3. What type of G protein?
  4. Agonist?
  5. Antagonist?
A 
1. smooth muscle- relax
skeletal muscle- relax
liver- glycogenolysis
3. Gs (increase AC)
4. albuterol, terbutaline
5. Experimental (propanolol, metoprolol, atenolol)
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17
Q

For the cardiovascular system, the most important receptors are ______for the vessels and ______ for the heart.

A

a1 and b2 for the vessels

b1 for the heart

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18
Q 
What is the effect of NE on:
1. BP
2. Femoral blood flow
3. renal blood flow
4. PVR
5. myocardial contractile force
6. HR
7. CO
Include a brief reason why.
A
  1. Increase (a1)
  2. decrease (a1)
  3. decrease (a1)
  4. increase
  5. increase (b1)
  6. brief increase (b1) then decrease (reflex)
  7. no change
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19
Q 
What is the effect of epi on:
1. BP
2. Femoral blood flow
3. renal blood flow
4. PVR
5. myocardial contractile force
6. HR
7. CO
Include a brief reason why.
A
  1. increase (a1) but not as much as NE because there is b2 relaxation component too
  2. increase because of the large b2 component
  3. decrease (largely a1)
  4. increase but not as much as NE
  5. increase (b1)
  6. increase (b1)
  7. increase
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20
Q 
What is the effect of isoproterenol on:
1. BP
2. Femoral blood flow
3. renal blood flow
4. PVR
5. myocardial contractile force
6. HR
7. CO
Include a brief reason why.
A
  1. decrease (b2)
  2. increase (b2)
  3. increase (b2)
  4. decrease
  5. increase (b1)
  6. increase (b1)
  7. increase to compensate for low BP
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21
Q 
What is the effect of phenylephrine on:
1. BP
2. Femoral blood flow
3. renal blood flow
4. PVR
5. myocardial contractile force
6. HR
7. CO
Include a brief reason why.
A
  1. increase (a1)
  2. decrease (a1)
  3. decrease (a1)
  4. increase
  5. same/slight decrease (no b1 stimulation)
  6. decrease as reflex to increased PVR
  7. decreased
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22
Q

What type of drug is phenylephrine? What are the results of giving it intravenously?

A

It is an a1 specific agonist. If given by IV it will vasoconstrict, increasing PVR with a rise in systolic and diastolic pressure.
The rise in pressure leads to baroreceptor reflex which will decrease HR due to increased vagal tone.

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23
Q

What type of drug is clonidine? What is its mode of action?

What three substances does clonodine reduce from plasma concentration?

A

It is an a2 specific agonist. It acts on receptors in the brainstem to turn down sympathetic signals. This results in decreased PVR in the standing position and decreased HR and stroke volume in the supine position.

It decreases renin aldosterone and NE

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24
Q

What type of drug is dobutamine? What are the results you would expect to see upon administration?

A

It is a b1 agonist.

It has positive ionotropic and chronotropic actions on the heart

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25
Q

What effect predominates when dobutamine is given over isoproterenol?

A

Isoproterenol is non-selective b agonist so it will alsp have a vasodilation effect. This will cause it to have a smaller ionotropic effect due to the decreased PVR.
Dobutamine will have a predominant ionotropic effect bc PVR will remain unchanged

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26
Q

Any b-adrenergic agonist comes at the cost of increased ______________.

A

oxygen consumption because b1 will cause the heart to pump harder and faster

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27
Q

What type of drug is isoproterenol?

When given IV what are the results?

A

B1+B2 agonist
When given by IV it will increase HR and contractility and vasodilate the vessels.
This decreases PVR especially in mesenteric, renal and skeletal vessels.
As a reflex, the vessels will reinforce the ionotropic effects on the heart

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28
Q

What does isoproterenol do the the systolic and diastolic BP?

A

Because of its b1 effects, HR and contractility will increase.
Because of b2, vasodilation renally mesenterically and in skeletal muscle will cause reflex that reinforces the increase in HR and contractility.
CO will increase as a result, so systolic BP will stay the same or rise, and because of the dilation, diastolic BP will fall

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29
Q

What is a negative effect of using isproterenol? Patients with _________ should especially not use this drug.

A

It can cause arrythmia
Patients with cardiac ischemia should not use isoproterenol because the increased work of the heart will require more oxygen consumption and it is already not getting enough

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30
Q

At low doses, epi effects __________ receptors the most and the responses resemble what drug?

A

B1 and B2 the most so the response resembles that of isoproterenol

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31
Q

AT higher doses of epi _________ receptors come into play and the effects of ____ and _____ predominate.

A

a1 come into play and the effects of a1 and b1 predominate.
You see positive ionotropic and chronotropic effects and an increased CO with elevated systolic and diastolic pressure due to vessel constriction and increased CO

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32
Q

What at the receptors effected by NE? What cardiovascular results would you see?

A

a1, b1, a2 so you would see an increase in BP (a1)

CO may be unchanged because of b1 agonistic activity

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33
Q

When given at low doses, dopamine effects ______ recepters located in ___________ and ___________ vascular beds.

A

D1 receptors in renal and mesenteric vascular beds and in the CNS

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34
Q

What type of G protein are D1 receptors coupled to? What response would you expect from stimulation?

A

Gs (increased AC) so you would expect relaxation and vasodilation

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35
Q

Describe the changes in action of dopamine as you move to higher and higher doses.

A

first, D1 with vasodilation of renal, mesenteric arterial beds and CNS activity
B1 will then stimulate HR and contractility increasing CO and systolic BP with little change in PVR
a1 is then activated which increases PVR and reduces CO

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36
Q

What would be a clinical situation when you would use dopamine for cardiac effects?

A

If there is compromised renal profusion due to circulatory shock. D1 receptors would vasodilate and increase blood flow to the kidneys

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37
Q

Which agonists are the most powerful bronchodilators?

A

B2 agonists

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38
Q

The effects of B2 agonists in the lungs are to _____________________ and ____________________ but they do NOT reduce____________________.

A

they decrease airway resistance and suppress release of inflammatory mediators but they do NOT reduce hyperresponsiveness of the bronchial

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39
Q

What is the benefit of using a B2 specific agonist over isoproterenol or epinephrine?

A

When a b2 agonist is inhaled, you get relax response from the bronchi with minimal effect of cardio system

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40
Q

What is the difference between albuterol and salmeterol?

A

Salmeterol has a longer half life (12 hours or more)

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41
Q

In addition to respiratory effects, what else are B2 specific agonists used for?

A

Since they relax smooth muscle they are used to stop premature labor by reducing contractions.
Ritodrine and terbutaline are the drugs of choice.

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42
Q

What kind of drug is ritodrine? What does it do?

A

It is a b2 agonist and is used to stop premature labor

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43
Q

How might b2 agonists be used to treat patients with diabetes?

A

b2 receptors can be found on the liver and do glycogenolysis. They also can do glycogenolysis on skeletal muscle.
B2 also enhances insulin secretion on the pancreas while a2 stops secretion (a2 predominates with epi)

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44
Q

What are the five main situations when phenylephrine could be used?

A
  1. local vasoconstriction
  2. nasal decongestion
  3. opthalmically
  4. Paroxysmal atrial tachycardia
  5. hypotensive states
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45
Q

How is phenylephrine used as a vasoconstrictor?

A
  1. It is used in local anesthesia to limit the distribution and prolong the duration of the anesthetic
  2. controls local bleeds
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46
Q

Why would you use phenylephrine to treat nasal congestion?

What is the negative side effect?

A

Because a1 receptors would allow the shrinkage of mucus membranes in patients with acute rhinitis.

The side effect is rebound hyperemia as well as urinary retention by constriction of trigone and sphincter

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47
Q

How is phenylephrine used opthalamically?

A
  1. It is a pupil dilator without cyclopegia (ciliary muscle paralysis)
  2. reduces red eye when used topically by constricting blood vessels in the eye
48
Q

How does phenylephrine treat tachycadia?

A

It raises the BP and sets of the vagal reflex which will slow the heart

49
Q

You would use phenylephrine to treat ______tension associated with paralysis of ___________.

A

hypotension associated with paralysis of the sympathetic nervous system

50
Q

What is hypovolemic shock?

What are the two major ways a patient can get this?

A

When there is inadequate filling of the ventricles because of inadequate return to the heart.

  1. decreased blood volume (burns, ascites, sepsis)
  2. Obstruction of venous return
51
Q

What are factors that can lead to decreased blood volume (and hypvolemic shock)?

A
  1. external or internal hemorrhage
  2. loss of fluid from vascular compartment (ascites, burns, sepsis)
  3. loss of fluid by GI (vomit/diarrhea)
  4. diabetes insipitus
52
Q

What is the reflex response to hypovolemic shock? How does this dictate what drugs you should use to treat?

A

Reflex is increased sympathetic response to perfuse blood: vasoconstrict, tachycardia, renin-angio-aldosterone to retain fluid
You don’t want to constrict vessels MORE to compromise perfusion so you do NOT want to give a1. You would try to replace the lost volume with fluid comparable to that which was lost and use B1 to circulate the fluid quicker to the tissues

53
Q

What is cardiogenic shock?

How do you treat?

A

inadequate cardiac output due to impaired contractile function (infarct, heart failure, cardiomyopathy) etc
Treat by maintaining adequate fluid and reduce ventricular afterload by using vasodilators.
Use b1 as needed

54
Q

What is hyperdynamic shock?

A

Fall in PVR caused by:

  1. sepsis
  2. anaphylaxis
  3. adrenal insufficiency
  4. neurological disorders
55
Q

How does a patient presenting with hyperdynamic shock look different from one with hypovolemic shock?

A

dymanic- they look warm and perfused but then when CO can’t keep up with decreased PVR, they will progress to hypovolemic
hypovolemic look pale due to lack of blood volume

56
Q

What is anaphylactic shock?

A

A hypersensitivity reaction characterized by bronchospasm, edema of mucous membranes, angioedema and cardio collapse

57
Q

How do you classically treat anaphylactic shock

A

epi to vasoconstrict to reverse edema and cause positive ionotropic activity

58
Q

What is used to treat septic shocK?

A

Antibiotics
Activated protein C
a and b agonists as needed by the situation

59
Q

What is clonidine mostly used for ? How is it administered?

Who would NOT be able to use this drug?

A

It is used to treat hypertension by reducing sympathetic tone on vessels through its action on a2 in the brainstem.

It is orally administered or transdermal patch (so compliance shouldnt be an issue)

It would not be effective to reduce hypertension in someone who has has a spinal transection.

60
Q

What are the 5 main adverse effects of clonidine?

A
  1. if given IV it actually increases BP
  2. dry mouth
  3. bradycardia
  4. postural hypotension
  5. withdraw (headache, tachycardia, hypertension )***
61
Q

How can clonidine test for pheochromocytoma?

A

Pheo is an adrenal tumor that secretes excess NE and epi.
Clonidine damps down sympathetics.
If the patient has pheo, it will be INSENSITIVE to clonidine

62
Q

How long after initiation of clonidine with transdermal patch can you measure its efficacy?

A

4-5 half lives so about 2 days

63
Q

What should you warn patients of before using clonidine? Who should not receive this drug?

A

Warn of the withdrawal effects and do not give to non-compliant or irresponsible individuals

64
Q

When would you give a patient dobutamine?
What are the contraindications?
What is the half life?

A

When they are coming out of cardiac surgery, have acute congestive heart failure, myocardial infarct

Contraindications: ischemia because of increased o2 demand

It only has a 2 minute half life so it provides short term increase in ionotropic and chronotropic activity

65
Q

What are the short acting b2 agonists?

A

albuterol and terbutaline

66
Q

How are b2 agonists administered? What is the benefit?

The ideal drug should be absorbed ___________ in the GI tract or ___________ extensively.

A

They are inhaled so there is minimized cardiovascular and other complications.
They should be poorly absorbed in GI tract and metabolized extensively during first pass of the liver

67
Q

What are the benefits of :

  1. inhalers
  2. nebulizers
  3. spacers in a metered dose inhaler
A
  1. they are inexpensive and portable
  2. they do not require hand-breath coordination and can be given via face mask
  3. spacers allow limitted deposition of larger particles
68
Q

What is the difference between a metered-dose and a dry-powder inhaler?

A

MEtered dose needs a propellant and dry-powdered does not

69
Q

What is the time of ons?set and duration for albuterol and terbutaline?
What is the time and duration of salmeterol?

A

30 minutes for max dilation and acts for 3-6 hours

Salmeterol has a delayed onset but lasts for 12 hours

70
Q

Why would excessive use of a b2 agonist cause mortality?

A
  1. IT exacerbates bronchial reactivity

2. it desensitizes the b receptors

71
Q

What is the recommended usage for short duration b2 agonists?

A

use them when experiencing an acute bronchospasm

72
Q

What is the recommended usage for long-acting b2 agonists (salmeterol)?

A

use alone or with glucocorticoids to control persistent asthma or nocturnal asthma symptoms

73
Q

When would ritodrine be used?
How is it administered?
What are side effects?

A

To stop premature labor in a pregnancy that was between 20 and 36 weeks. It is given IV then orally.

Since it is a b2 agonist, it will induce tachycardia (due to low PVR and reflex) renin secretion and salt retention

74
Q

What is epinephrine reversal?

A

When given an alpha blocker (phenylbenzamine) epinephrine will cause vasodilation (because of b2 effect).
If there was no a-blocker, there will be vasoconstriction due to a1 effect

75
Q

What is tachyphylaxis?

A

When repeated uses of indirectly acting sympathomimetic amines deplete the supply of NE

76
Q

Indirect acting sympathomimetic amines have action similar to ____ only ______in onset and ____ in duration.

A

NE only slower in onset and longer in duration

77
Q

How do sympathomimetic drugs gain access to the presynaptic terminal to be able to release NE?
What drugs act as sympathomimetic amines?

A

They are taken up by the same reuptake pathway as NE

Tyramine
amphetamine
methyphenidate
ephedrine

78
Q

What drugs actions are blocked by cocaine and TCA?

A

tyramine, amphetamine, methyphenidate, ephedrine and NE because they block the uptake into the presynaptic terminal

79
Q

Where is tyramine found?

A

In aged cheese, chicken liver, fermented sausage, pickled/smoked fish, red wine

80
Q

What interaction is there between MAOI and tyramine?

A

Tyramine and MAOI both will increase release of NE so they will potentiate each others actions.

This will increase NE action on a1, a2, b1 and will cause hypertension, MI and stroke

81
Q

Describe how epedrine works, and what it is used for.

A

It is an indirectly acting NE agonist (increased NE release)
It is used for asthma, colds, and performance enhancement
It is an alpha and beta agonist

82
Q

What allows amphetamines to be extremely long acting? Where can you see its affects?

A

It is lipid soluble and metabolically blocked. You see the effects in the cardiovascular system and CNS

83
Q

What are the cardiovascular effects of amphetamines?

A

They increase NE release so they will increase ionotropic and chronotropic action of the heart, vasoconstrict (increase BP) and as a reflex cause brachycardia

84
Q

What are the CNS effects of amphetamines?

How could an overdose present?

A

They increase NE and dopamine release so they promote wakefulness, alertness, elevation of mood, confusion, delerium
Overdose presents as convulsions, coma and cerebral hemorrhage.

85
Q

What is the effect of amphetamines on appetite?

A

it suppresses appetite which can lead to substantial abuse as a diet aid

86
Q

What is methylphenidate?

What are side effects?

A

Ritalin- it is an indirect sympathomimetic used to treat ADHD.
Side effects are insomnia, weight loss, anorexia
Because of this drug holidays are recommended

87
Q

How do most appetite suppression drugs (except fenfluramine) work?
How does fenfluramine work? What major side effect does it cause?

A

as indirectly- acting adrenergic agonists
(like amphetamine)

Fenfluramine cause 5HT depletion from CNS and act as agonists for some 5HT receptors. Because it depletes serotonin it can cause depression and pulmonary hypertension

88
Q

The fen-phen diet craze stopped when the Mayo Clinic linked it to what?

A

valvular heart disease where the valves got covered in plaque

89
Q

What kind of drug is methyldopa?

A

it is a prodrug that acts as an alpha2 agonist with anti-hypertensive effects

90
Q

What is a false neurotransmitter?

What are two examples?

A

When a drug besides the neurotransmitter is packaged into the vesicles and released upon stimulation.

  1. Methyldopa- a produg converted to methylnorepinephrine by the same enzyme that converts DOPA to NE. a-methylNE is packaged in vesicles and released with stimulation
  2. Guanethidine inhibits NE release and is released upon nerve stimulation through vesicles
91
Q

What are the actions of methyldopa?

A

When it is converted to a-methylNE and released from vesicles upon nerve stimulation it will act as an a2 agonist. Thus it:
decreases PVR and lowers CO to treat hypertension but can cause moderate othostatic hypotension

92
Q

How do gaunethidine enter the nerve terminal?
Once it is there, what does it do?

What is the ultimate effect?

A

They are taken up by the NE reuptake transporters (like tyramine, amphetamine etc)
Once in the nerve terminal they bind to vesicles and prevent NE vesicle release OR is transported into vesicles to replace NE

The ultimate effect is blockage of NE and thus removal of sympathetic tone (hypotension, fluid retention, diarrhea)

93
Q

What is reserpine?

A

A drug that binds and inactivates neuronal storage vesicles blocking their ability to release NE, epi, dopamine, 5HT

Used to lower BP but must give a very low dose because of the side effects

94
Q

Metyrosine does what?

What is the only real thing it is used for?

A

Inhibits the formation of DOPA from tyrosine (rate limiting step in NE synthesis)
It is used in pheochromacytoma where an adrenal tumor over produces NE

95
Q

What is the general effect of a1 and a2 blockers?

A
  1. vasodilation, decreased PVR, decreased BP
  2. compensatory tachycardia and fluid retention (vagal and renin-angiotensin)
  3. relaxation of trigone and sphincter and vas deferens
96
Q

Why is tachycardia exaggerated with non-specific alpha antagonists?

A

a1 blockage will vasodilate causing reflex to increase HR

a2 blockage will stop the inhibition of Ach and NE release which will increase b1 activity to increase HR

97
Q

When a patient is given epi without an a blocker, what is the response?
What is the response of epi + alpha blocker?

A

Just epi- increased BP due to a1 tone being greater than b2 tone
Epi + a-blocker will decrease BP because the b2 relaxation will provide dominant tone

This is called epi reversal

98
Q

What are the general effects of a2 specific blockers?

A

If there is no a2 action, there will be less inhibition of NE release. NE will then cause:

  1. vasoconstriction (a1)
  2. increased HR/contractility (b1)
99
Q

What is the role of phenoxybenzamine?
How molecularly does it work?
What are the two main uses for it?

A
  1. It is a nonspecific a blocker.
    It acts as an alkylating agent that irreversibly blocks alpha receptors. The response lasts 3-4 days because to regain receptors they must be synthesized
  2. It inhibits the reuptake of NE at sympathetic neurons
    Its only real use is treating pheochromacytoma and to prepare patients for surgery
100
Q

What are the a1 specific blockers and what is their mode of action?

A

Tamusolin and Prazosin which will decrease PVR and decrease venous return

101
Q

Why is there less tachycardia with an a1 specific blockade (than with a non-selective blockade)?

A

a2 will be able to inhibit excessive NE release so there will still be tachycardia, but less bad.

102
Q

What is tamusolin used specifically to treat?

A

benign prostatic hypertrophy.relax bladder smooth muscle

103
Q

What is the main use of prazosin?

A

To reduce primary systemic hypertension used in combo with a b-blocker or diuretic.

104
Q

What is the main action of propanolol?

A

It is a beta blocker that blocks competitively so it will restrict action of endogenous or exogenous sympathomimetic amines
It is non-specific for b1 or b2 and is very lipophilic and enters CNS

105
Q

What is the dominant effect of a beta blocker?

A

reduces HR and decreases force of contraction (particularly during exercise or stress

It will decrease cardiac output and increase PVR (but in long term PVR returns to normal)

block catecholamine stimulated renin-excretion

Can cause bronchoconstriction

106
Q

What is the effect of b blockers on the kidneys?

A

It will decrease renin secretion (b1 effect)

107
Q

Why is a beta blocker not wise to use on a diabetic?

A

It may mask tachycardia which is a sign diabetics usually have to warn themselves of hypoglycemia

108
Q

What are metoprolol and atenolol? How are they different?

A

They are B1 specific antagonists
Metoprolol has a shorter half life and is able to get into the CNS
Atenolol has a longer half life and cant get into the brain

109
Q

What does carvedilol do?

A

It is a nonselective B blocker and an a1 blocker.

It is used to treat congestive heart failure

110
Q

What are the negative side effects of a beta blocker?

A
  1. CHF
  2. rebound effect with increased BP/HR
  3. bradyarrhythmia
  4. increased airway resistance
  5. decreased exercise tolerance
111
Q

b blocker is a good choice for patients with______ or ______ but a bad choice if the patient has _______, _____, _________/

A

Good for angina or tachycardia

Bad for asthma, diabetes, bradyarrythmias

112
Q

Administration of B blocker following infarct lowers incidence of death due to what two things?

A
  1. decreased cardiac rupture

2. preventing ventricular fibrillation

113
Q

What 7 clinical conditions benefit from b-blockers?

A
  1. hypertrophic cardiomyopathy
  2. Acute dissecting aortic aneurysm
  3. hyperthyroidism
  4. migraine prophylaxis
  5. panic attacks
  6. open angle glaucoma
  7. pheochromocytoma
114
Q

How do b-blockers help with hyperthyroidism?

A

thyroid hormone stimulates the transcription of b-adrenergic receptors so it blocks some to help with angina and hyperactivity

115
Q

How does b-blocker help treat open angle glaucoma?

A

It prevents formation of aqueous humor

Bugs and Drugs (21 decks)

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