Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Mo and Mik > m and m 14 - Adrenergic Agonists and Antagonists > Flashcards

m and m 14 - Adrenergic Agonists and Antagonists Flashcards

1
Q

What is the major neurotransmitter for the sympathetic nervous system? What is the sympathetic tissue that doesn’t use this neurotransmitter?

A

Norepinephrine. Only exception where NE isn’t released at the end organ is eccrine sweat glands

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the neurotransmitter for all the preganglionic sympathetic fibers and all the parasympathetic nervous system?

A

Acetylcholine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What spinal cord levels give rise to the sympathetic nervous system? The parasympathetic?

A

Sympathetic arises from T1-L3

Parasympathetic is cranio-sacral in distribution

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is a the major difference between the sympathetic and parasympathetic systems regarding location of the ganglion relative to the end organ innervated?

A

The sympathetic ganglion are usually paraspinal and thus very far from the end organ innervated, vs parasympathetic that are closer to the end organ

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

In what part of the sympathetic postganglionic nerve ending is norepi made? How is it released?

A

Made in cytoplasm, stored in vesicles and released by exocytosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the major mechanism for terminating the activity of NE? What is a drug class that blocks this activity

A

Reuptake - can be blocked by tricyclic antidepressants

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are two enzymes that metabolize NE?

A

Catechol-O-Methyltransferase

Monoamine oxidase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the rate limiting step in the synthesis of norepinephrine?

A

Hydroxylation of tyrosine to dopa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Norepinephrine is the precursor to epinephrine. Where does this conversion occur?

A

In the adrenal medilla

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the common end product of enzymatic metabolism of NE or epi?

A

Vanillylmandelic acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What type of receptors are adrenergic receptors?

A

GPCRs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the associated g-proteins for alpha 1, alpha 2 and the beta receptors?

A

Gq, Gi and Gs, respectively

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Where are alpha 1 receptors located? What is the effect of their activation?

A

Located in smooth muscle all across the body. Activation causes increase in intracellular calcium and muscle contraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the effect of alpha 1 agonists on

  • eye
  • lungs
  • vasculature
  • uterus
  • GI sphincters
A
  • eye - mydriasis (pupil dilation from contraction of radial eye muscles)
  • lungs - bronchoconstriction
  • vasculature - vasoconstriction
  • uterus - contractions
  • GI sphincters - constrictions of sphincters
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the effect of alpha 1 on insulin secretion and lipolysis?

A

It inhibits both of those processes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is effect of alpha 1 agonists on peripheral vascular resistance, afterload and blood pressure?

A

Increases all of them

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Are alpha 2 receptors presynaptic or postsynaptic? Where is the exception? What is the mechanism for its effect on NE?

A

Presynaptic (some post-synaptic is vascular smooth muscle)

Activation blocks adenylate cyclase activity, reduces calcium in the neuronal terminal, decreases release NE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is the net effect of stimulation of alpha 2 in the CNS?

A

Sedation and decreased sympathetic outflow (decreased BP and lower blood pressure)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

How many types of beta receptors are there? How does the potency of epi and NE compare with these receptors?

A

beta 1,2,3
NE and Epi equipotent on beta 1
Epi significantly more potent on beta 2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Where are beta 1 receptors located? What is the effect of their activation of chronotropy? dromotropy? inotropy?

A

Located on post synaptic membranes of the heart.

Activation increases chronotropy, dromotropy (conduction) and inotropy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Where are beta 2 receptor located?

A

Post synaptically on smooth muscles and gland cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is the effect of beta 2 activation on:

  • lungs
  • vasculature
  • uterus
  • bladder
  • gut
A

Causes relaxation of all these muscles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is the effect of beta 2 activation of glycogenolysis, lipolysis, gluconeogenesis and insulin release?

A

All increased / stimulated by beta-2 activation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What are the 2 known locations of beta 3 receptors?

A

Gall-bladder and brain adipose tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Activation of D1 causes vaso-[constriction/dilation] of 3 organ systems. What are they?

A

Vasoconstriction

Heart, kidneys and intestines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is the significance of D2 receptors in anesthesiology?

A

Thought to play a role in antiemetic actions of droperidol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What are the 2 mechanistic ways that indirect agonists of adrenergic receptors work?

A

Increased release or decreased reuptake of norepinephrine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

A patient who uses a monoamine oxidase inhibitor as an outpatient has intraoperative hypotension. What type of agonist [direct/indirect] should be used and why?

A

Should use direct agonist because the response to an indirect agonist is likely altered in this patient

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What is the chemical group that distinguishes catecholamines? What structures confer specificity?

A

The 3,4 dihydrobenzene structure

The R 1,2,3 side chains confer specificity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Why are isoproterenol and dobutamine “special” compared to the other catecholamines?

A

These are synthetic catecholamines that were developed after changing the side chains of the naturally occuring catecholamines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is the receptor target of phenylephrine? What is effect on SVR, BP, HR?

A

alpha 1 agonist
increases SVR and BP
Decreases HR (reflex bradycardia mediated by vagus nerve)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Phenylephrine can be used as a continuous infusion. What organ system may end up not getting enough blood flow? Why would you need to uptitrate dose of infusion?

A

Renal blood flow may go down

Tachyphylaxis a problem, may need to uptitrate dose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What are 3 uses of clonidine?

A

Antihypertensive
Negative chronotrope
Sedation / anxiolysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What is a possible advantage of clonidine from a circulation perspective? what is the mechanism?

A

It enhances intraoperative circulatory stability by decreasing catecholamine levels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What is the effect of clonidine on a regional anesthetic?

A

Clonidine will prolong the block duration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

3 possible benefits of intraoperative clonidine are?

A

Decreased post op shivering
Inhibition of opioid induced muscle rigidity
Attenuation of opioid withdrawal symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Which has higher affinity at the alpha 2 receptor, clonidine or dexmeditomidine? Which is more selective (compared to alpha 1)? Which has a longer half life?

A

Dexmeditomidine has higher affinity and selectivity

Clonidine has higher half life

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

The sedative and analgesic effects of dexmeditomidine are mediated by alpha 2 receptors located where?

A

Brain (locus ceruleus) and spinal cord

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

True or false - both clonidine and dexmeditomidine can reduce anesthetic requirement?

A

True

40
Q

Dexmeditomidine is useful for the sedation of patient undergoing awake fiberoptic intubation, or needing post-op sedation. What property of this drug make it useful in this setting?

A

It is a sedative that has minimal ventilatory depressive effects

41
Q

What is the effect of abrupt discontinuation of clonidine or dexmeditomidine after long term use? Mechanism?

A

Hypertensive crisis

Mechanism is upregulation of adrenergic receptors, leading to supersensitization

42
Q

What is the time line for hypertensive crisis after discontinuation of dexmeditomidine? Mechanism? Sooner or later than clonidine?

A

Hypertensive crisis can occur after using dex for 48 hours
Because of the higher affinity for alpha 2
Way faster than with clonidine

43
Q

What is the mechanism of epinephrine increasing myocardial oxygen demand?

A

Increases contractility and heart rate

44
Q

Epinephrine [increases/decreases] coronary perfusion pressure. Mechanism?

A

Increases perfusion pressure by increasing aortic diastolic pressure (diastole is when the coronaries are perfused)

45
Q

What are 3 known complications of epinephrine?

A

Cerebral hemorrhage
Coronary ischemia
Ventricular Dysrhythmias (potentiated by volatile anesthetics, especially halothane)

46
Q

What is the dosage of epinephrine for anaphylaxis?

A

100-500 mcg

47
Q

Ephedrine and Epi have similar actions. Which is more potent? Longer duration of action?

A

Epinephrine is more potent

Ephedrine has a longer duration of action

48
Q

True or false - ephedrine is a MAC sparing agent?

A

False - it stimulates the CNS, will therefore cause more anesthetic to be used (Raises the MAC)

49
Q

What is the proposed mechanism of the indirect agonist properties of ephedrine?

A

Peripheral postsynaptic NE release or by inhibitionr of NE re-uptake

50
Q

What are the preferred vasopressors for obstetric use? Why?

A

Phenylephrine and ephedrine - these 2 anesthetics are believed to not reduce uterine blood flow.
** Phenylephrrine preferred because of faster onset, shorter duration of action, better titratability and maintenance of fetal ph)

51
Q

What are the 3 adrenergic subtypes that Norepi has effects on?

A

Works on beta 1, alpha 1 and 2. Minimal effect on beta 2

52
Q

What is the effect norepi on cardiac output? Why?

A

No significant increase in CO. Despite its beta 1 effects, it will also increase systolic and diastolic BP, causing reflex bradycardia

53
Q

What is the thinking re: norepinephrine in shock?

A

Not used because it decreases renal and splanchnic blood flow and increases myocardial oxygen demand

54
Q

What is the net effect of low dose dopamine?

A

Vasodilates the renal vasculature

Promotes naturesis and diureses

55
Q

What are the receptors that are targeted as you increase the doses of dopamine? What is the net effect?

A

DA-1 - vasodilates renal vasculature
Beta 1 - increases contractility, HR and CO
Alpha 1 - increases peripheral vascular resistance and decreases renal blood flow

56
Q

What is the basis of the indirect effects of dopamine?

A

Can cause release of norepinephrine from the presynaptic nerve ganglion

57
Q

When dopamine is used to treat patients in shock (improves CO, BP and maintain renal function), what else is co-administered to maximize cardiac output?

A

Usually used with a vasodilator (e.g. nitroglycerin or nitroprusside) to reduce afterload and further improve cardiac output

58
Q

What are 2 known side effects of dopamine that may limit its use, especially in shock patients?

A

It increases chronotropy

It is pro-arrythmic

59
Q

What is the receptor targeted by isoproterenol? What is the effect on HR, contractility, CO, peripheral vascular resistance and diastolic BP?

A

Pure beta agonist
Will increase HR, contractility and CO
Will decrease peripheral vascular resistance and diastolic BP (via beta-2 mechanism)

60
Q

Why is a pure beta agonist, e.g. isoproterenol a poor inotropic choice in most situations?

A

While it will increase HR, myocardial O2 demand will increase while O2 supply will fall (will drop diastolic BP, perfusion of coronaries will drop)

61
Q

Dobutamine binds which type of adrenergic receptor? Is there any subtype selectivity?

A

Will bind beta 1 and beta 2, more selective for beta 1 over beta 2

62
Q

What is the effect of dobutamine on

  • CO
  • contractility
  • peripheral vascular resistance
  • LV filling pressures
  • Coronary blood flow
A
  • CO -> increases
  • contractility -> increases
  • peripheral vascular resistance -> decreases (beta 2)
  • LV filling pressures -> decreases
  • Coronary blood flow -> increases
63
Q

Dobutamine is thought to be a good choice for the treatment of patients with CHF and CAD, especially if there is increased peripheral vascular resistance. Why?

A

It has a “favorable effect on myocardial oxygen balance” i.e. increases contractility and CO while increasing coronary blood flow

64
Q

What is dopexamine? How is it different from dopamine?

A

It is a structural analogue of dopamine, but less beta -1 activity and less alpha 1 effects. Still has it “pro-renal” effects

65
Q

What are the receptors affected by fenoldopam?

A

It is able to bind D1 as well as dopamine. It has little effect on the alpha, beta and D2 receptors

66
Q

What is the effect of fenoldopam on

  • peripheral vascular resistance
  • Renal blood flow
  • diuresis
  • natriuresis
A

Decreases PVR, increases everything else

67
Q

What type of patient (i.e. what constellation of circumstances) will particularly benefit from fenoldopam?

A

Patient undergoing aortic aneurysm repair with high risk of renal impairment.
** can also be used for severely hypertensive patients with suspected renal impairment **

68
Q

What is an adrenergic agent that is indicated for prevention of contrast media induced nephropathy?

A

Fenoldopam

69
Q

Phentolamine is a [competitive/non-competitive] blocker of what receptor(s)?

A

Competitive alpha-1 and alpha 2

70
Q

What is the net effect of phentolamine use on the cardiovascular system (2 things)?

A
  • peripheral vasodilation, decrease in BP (alpha 1 block)
  • Reflex tachycardia (alpha 2 block and response to decreased BP - activation of alpha-2 decreases release of NE, phentolamine does opposite, therefore more NE released)
71
Q

What 2 side effects limit the use of phentolamine in the tx of hypertension from too much alpha stimulation?

A

Postural hypotension

Reflex tachycardia

72
Q

What are the targets of prazosin and phenoxybenzamine?

A

Both are also alpha antagonists, phenoxybenzamine is a non-competitive agent

73
Q

What are the receptors blocked by labetalol? What is the net effect on the CV system?

A

Alpha 1, beta 1 and beta 2. Will decrease BP with minimal effect on HR and cardiac output

74
Q

What are 3 potential (reported) side effects of labetalol?

A

Bronchospasm
Paradoxical hypertension
LV failure

75
Q

Why should beta-2 blockers be used with caution in patients with peripheral vascular disease?

A

Blocking of beta 2 can theoretically reduce blood flow to the peripheral vasculature (blocking by beta 2)

76
Q

What is the effect of beta 2 blockers on patients with glaucoma?

A

Can theoretically reduce intraoccular pressure in patients with glaucoma

77
Q

What are the 3 beta blockers that are thought to be selective for beta 1? Which is a mixed antagonist? Which is more beta 2?

A

beta 1 - metop, esmolol and atenolol

mixed - labetalol and propranolol

78
Q

What 3 beta blockers are metabolized by the liver? which is metabolized unchanged by kidneys? Which is metabolized in blood?

A

Liver - propranolol, metoprolol and labetalol
Kidneys - atenolol
Blood - esmolol

79
Q

What is the major effect of esmolol on CV system?

A

Blocks increase in HR to lesser extent, BP. Beta 1 selective

80
Q

What happens to esmolol as higher doses are used in patients?

A

At higher doses, will now become less selective for beta 1 and will start blocking beta 2 in the smooth muscles and bronchioles

81
Q

How is esmolol metabolized?

A

Hydrolyzed by red blood cell esterases

82
Q

What are 4 contraindications for esmolol?

A

Sinus bradycardia
More than 1st degree heart block
Heart failure
Cardiogenic shock

83
Q

What is the receptor target of metoprolol? Does it have intrinsic sympathomimetic activity?

A

Beta 1 selective. No intrinsic sympathomimetic activity

84
Q

What is the receptor target of propranolol?

A

Beta 1 and beta 2

85
Q

What is the mechanism by which propranolol decreases BP (3)?

A

Decreased contractility
Decreased HR
Decreased renin release
(all above leads to decreased cardiac output and myocardial oxygen demand)

86
Q

What beta blocker has the following characteristics?

  • slows AV conduction and stabilizes cardiac membranes
  • slows ventricular response in SVT
  • Blocks beta effects in thyrotoxicosis and pheochromocytoma?
A

Propranolol

87
Q

What are possible side effects of propranolol?

A

Bronchospasm
CHF
Bradycardia
AV block

88
Q

What beta blocker may worsen the myocardial depression of halothane and unmask the negative inotropic characteristics of indirect cardiac stimulants?

A

Propranolol

89
Q

What class of drug, when used with propranolol can synergistically depress HR, contractility and AV conduction?

A

Calcium channel blockers

90
Q

What is the receptor target of nebivolol? What is unique about it?

A
  • Highly beta 1 selective

- Unique in that it can directly cause vasodilation via stimulation of endothelial nitric oxide synthase

91
Q

What is the receptor target of carvedilol? What are its inducations?

A

Mixed alpha and beta blocker

Indicated for CHF from cardiomyopathy, LV dysfunction after MI and hypertension

92
Q

True or false - in a patient already on beta blockers, they should be asked to stop this medication before surgery?

A

False. These shouldn’t be stopped if pateints are using for tx of angina, symptomatic arrythmias, HF, HTN

93
Q

What are potential complications of stopping beta blockers? What is the time line? Mechanism?

A

HTN, tachycardia and angina
24-48 hours
Possible upregulation

94
Q

What is a pheochromocytoma?

A

An adrenal medulla tumor of chromaffin tissue that makes NE and epi

95
Q

How is pheochromocytoma diagnosed?

A

Urinary excretion of vanillylmandelic acid is measure. Usually high in these patients

96
Q

What is the perioperative drug of choice for treatment of pheochromocytoma?

A

Phenoxybenzamine

97
Q

Why should the following drugs be avoided in a patient with pheochromocytoma?
Ketamine
Halothane
Vagolytics (anticholinergics and pancuronium)

A

Ketamine - a sympathomimetics
Halothane - sensitizes myocardium to arrhythmogenic effects of epinephrine
Vagolytics - will tip balance to increased tone

Mo and Mik (9 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions