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Adrenergics Flashcards

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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
What effect predominates when dobutamine is given over isoproterenol?
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
26
Any b-adrenergic agonist comes at the cost of increased ______________.
oxygen consumption because b1 will cause the heart to pump harder and faster
27
What type of drug is isoproterenol? | When given IV what are the results?
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
28
What does isoproterenol do the the systolic and diastolic BP?
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
29
What is a negative effect of using isproterenol? Patients with _________ should especially not use this drug.
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
30
At low doses, epi effects __________ receptors the most and the responses resemble what drug?
B1 and B2 the most so the response resembles that of isoproterenol
31
AT higher doses of epi _________ receptors come into play and the effects of ____ and _____ predominate.
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
32
What at the receptors effected by NE? What cardiovascular results would you see?
a1, b1, a2 so you would see an increase in BP (a1) | CO may be unchanged because of b1 agonistic activity
33
When given at low doses, dopamine effects ______ recepters located in ___________ and ___________ vascular beds.
D1 receptors in renal and mesenteric vascular beds and in the CNS
34
What type of G protein are D1 receptors coupled to? What response would you expect from stimulation?
Gs (increased AC) so you would expect relaxation and vasodilation
35
Describe the changes in action of dopamine as you move to higher and higher doses.
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
36
What would be a clinical situation when you would use dopamine for cardiac effects?
If there is compromised renal profusion due to circulatory shock. D1 receptors would vasodilate and increase blood flow to the kidneys
37
Which agonists are the most powerful bronchodilators?
B2 agonists
38
The effects of B2 agonists in the lungs are to _____________________ and ____________________ but they do NOT reduce____________________.
they decrease airway resistance and suppress release of inflammatory mediators but they do NOT reduce hyperresponsiveness of the bronchial
39
What is the benefit of using a B2 specific agonist over isoproterenol or epinephrine?
When a b2 agonist is inhaled, you get relax response from the bronchi with minimal effect of cardio system
40
What is the difference between albuterol and salmeterol?
Salmeterol has a longer half life (12 hours or more)
41
In addition to respiratory effects, what else are B2 specific agonists used for?
Since they relax smooth muscle they are used to stop premature labor by reducing contractions. Ritodrine and terbutaline are the drugs of choice.
42
What kind of drug is ritodrine? What does it do?
It is a b2 agonist and is used to stop premature labor
43
How might b2 agonists be used to treat patients with diabetes?
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)
44
What are the five main situations when phenylephrine could be used?
1. local vasoconstriction 2. nasal decongestion 3. opthalmically 4. Paroxysmal atrial tachycardia 5. hypotensive states
45
How is phenylephrine used as a vasoconstrictor?
1. It is used in local anesthesia to limit the distribution and prolong the duration of the anesthetic 2. controls local bleeds
46
Why would you use phenylephrine to treat nasal congestion? | What is the negative side effect?
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
47
How is phenylephrine used opthalamically?
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
How does phenylephrine treat tachycadia?
It raises the BP and sets of the vagal reflex which will slow the heart
49
You would use phenylephrine to treat ______tension associated with paralysis of ___________.
hypotension associated with paralysis of the sympathetic nervous system
50
What is hypovolemic shock? | What are the two major ways a patient can get this?
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
What are factors that can lead to decreased blood volume (and hypvolemic shock)?
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
What is the reflex response to hypovolemic shock? How does this dictate what drugs you should use to treat?
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
What is cardiogenic shock? | How do you treat?
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
What is hyperdynamic shock?
Fall in PVR caused by: 1. sepsis 2. anaphylaxis 3. adrenal insufficiency 4. neurological disorders
55
How does a patient presenting with hyperdynamic shock look different from one with hypovolemic shock?
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
What is anaphylactic shock?
A hypersensitivity reaction characterized by bronchospasm, edema of mucous membranes, angioedema and cardio collapse
57
How do you classically treat anaphylactic shock
epi to vasoconstrict to reverse edema and cause positive ionotropic activity
58
What is used to treat septic shocK?
Antibiotics Activated protein C a and b agonists as needed by the situation
59
What is clonidine mostly used for ? How is it administered? | Who would NOT be able to use this drug?
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
What are the 5 main adverse effects of clonidine?
1. if given IV it actually increases BP 2. dry mouth 3. bradycardia 4. postural hypotension 5. withdraw (headache, tachycardia, hypertension )***
61
How can clonidine test for pheochromocytoma?
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
How long after initiation of clonidine with transdermal patch can you measure its efficacy?
4-5 half lives so about 2 days
63
What should you warn patients of before using clonidine? Who should not receive this drug?
Warn of the withdrawal effects and do not give to non-compliant or irresponsible individuals
64
When would you give a patient dobutamine? What are the contraindications? What is the half life?
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
What are the short acting b2 agonists?
albuterol and terbutaline
66
How are b2 agonists administered? What is the benefit? | The ideal drug should be absorbed ___________ in the GI tract or ___________ extensively.
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
What are the benefits of : 1. inhalers 2. nebulizers 3. spacers in a metered dose inhaler
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
What is the difference between a metered-dose and a dry-powder inhaler?
MEtered dose needs a propellant and dry-powdered does not
69
What is the time of ons?set and duration for albuterol and terbutaline? What is the time and duration of salmeterol?
30 minutes for max dilation and acts for 3-6 hours | Salmeterol has a delayed onset but lasts for 12 hours
70
Why would excessive use of a b2 agonist cause mortality?
1. IT exacerbates bronchial reactivity | 2. it desensitizes the b receptors
71
What is the recommended usage for short duration b2 agonists?
use them when experiencing an acute bronchospasm
72
What is the recommended usage for long-acting b2 agonists (salmeterol)?
use alone or with glucocorticoids to control persistent asthma or nocturnal asthma symptoms
73
When would ritodrine be used? How is it administered? What are side effects?
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
What is epinephrine reversal?
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
What is tachyphylaxis?
When repeated uses of indirectly acting sympathomimetic amines deplete the supply of NE
76
Indirect acting sympathomimetic amines have action similar to ____ only ______in onset and ____ in duration.
NE only slower in onset and longer in duration
77
How do sympathomimetic drugs gain access to the presynaptic terminal to be able to release NE? What drugs act as sympathomimetic amines?
They are taken up by the same reuptake pathway as NE Tyramine amphetamine methyphenidate ephedrine
78
What drugs actions are blocked by cocaine and TCA?
tyramine, amphetamine, methyphenidate, ephedrine and NE because they block the uptake into the presynaptic terminal
79
Where is tyramine found?
In aged cheese, chicken liver, fermented sausage, pickled/smoked fish, red wine
80
What interaction is there between MAOI and tyramine?
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
Describe how epedrine works, and what it is used for.
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
What allows amphetamines to be extremely long acting? Where can you see its affects?
It is lipid soluble and metabolically blocked. You see the effects in the cardiovascular system and CNS
83
What are the cardiovascular effects of amphetamines?
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
What are the CNS effects of amphetamines? | How could an overdose present?
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
What is the effect of amphetamines on appetite?
it suppresses appetite which can lead to substantial abuse as a diet aid
86
What is methylphenidate? | What are side effects?
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
How do most appetite suppression drugs (except fenfluramine) work? How does fenfluramine work? What major side effect does it cause?
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
The fen-phen diet craze stopped when the Mayo Clinic linked it to what?
valvular heart disease where the valves got covered in plaque
89
What kind of drug is methyldopa?
it is a prodrug that acts as an alpha2 agonist with anti-hypertensive effects
90
What is a false neurotransmitter? | What are two examples?
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
What are the actions of methyldopa?
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
How do gaunethidine enter the nerve terminal? Once it is there, what does it do? What is the ultimate effect?
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
What is reserpine?
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
Metyrosine does what? | What is the only real thing it is used for?
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
What is the general effect of a1 and a2 blockers?
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
Why is tachycardia exaggerated with non-specific alpha antagonists?
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
When a patient is given epi without an a blocker, what is the response? What is the response of epi + alpha blocker?
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
What are the general effects of a2 specific blockers?
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
What is the role of phenoxybenzamine? How molecularly does it work? What are the two main uses for it?
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
What are the a1 specific blockers and what is their mode of action?
Tamusolin and Prazosin which will decrease PVR and decrease venous return
101
Why is there less tachycardia with an a1 specific blockade (than with a non-selective blockade)?
a2 will be able to inhibit excessive NE release so there will still be tachycardia, but less bad.
102
What is tamusolin used specifically to treat?
benign prostatic hypertrophy.relax bladder smooth muscle
103
What is the main use of prazosin?
To reduce primary systemic hypertension used in combo with a b-blocker or diuretic.
104
What is the main action of propanolol?
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
What is the dominant effect of a beta blocker?
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
What is the effect of b blockers on the kidneys?
It will decrease renin secretion (b1 effect)
107
Why is a beta blocker not wise to use on a diabetic?
It may mask tachycardia which is a sign diabetics usually have to warn themselves of hypoglycemia
108
What are metoprolol and atenolol? How are they different?
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
What does carvedilol do?
It is a nonselective B blocker and an a1 blocker. | It is used to treat congestive heart failure
110
What are the negative side effects of a beta blocker?
1. CHF 2. rebound effect with increased BP/HR 3. bradyarrhythmia 4. increased airway resistance 5. decreased exercise tolerance
111
b blocker is a good choice for patients with______ or ______ but a bad choice if the patient has _______, _____, _________/
Good for angina or tachycardia Bad for asthma, diabetes, bradyarrythmias
112
Administration of B blocker following infarct lowers incidence of death due to what two things?
1. decreased cardiac rupture | 2. preventing ventricular fibrillation
113
What 7 clinical conditions benefit from b-blockers?
1. hypertrophic cardiomyopathy 2. Acute dissecting aortic aneurysm 3. hyperthyroidism 4. migraine prophylaxis 5. panic attacks 6. open angle glaucoma 7. pheochromocytoma
114
How do b-blockers help with hyperthyroidism?
thyroid hormone stimulates the transcription of b-adrenergic receptors so it blocks some to help with angina and hyperactivity
115
How does b-blocker help treat open angle glaucoma?
It prevents formation of aqueous humor
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